Macular Degeneration Therapy

Tiny Existing Excitement May Show to be An effective Therapy with regard to Macular Degeneration.

2011-01-28T06:10:00.000-08:00

Human cells may not be unlike electric batteries. They from time to time have small energy retailers or can’t hold vigor. Micro Present-day Stimulation Remedy provides your cells with all the “energy” it takes, similar in order to recharging a new battery. Studies in addition have shown this MCS Remedy increases microcirculatory circulation, increases ATP concentrations plus stimulates amino acidity and source of nourishment concentrations directly into cells.

Every located cell inside body has a power charge. It is theorized that a part of what creates macular degeneration is usually a loss with the energy source inside cell, or losing the electrical charge. As being a flashlight will not likely work without getting a charged battery pack, the photoreceptors inside retina will not likely function not having an energy source. MCS Remedy is shown to increase the energy source within your cell.

This Macular Degeneration Foundation identified in starting pre-clinical trials by groundbreaking ophthalmologists plus researchers this micro present-day stimulation therapy can boost visual acuity, sharpness plus color perception in 68 percentage of individuals with dry out macular weakening and 58 percent of those with your wet kind. Reports from Russia advocate similar benefits.

A review published by way of Dr. Merrell J. Allen plus Dr. Leland N. Michael eligible Nutritional By using supplements, Electrical Excitement and Age Related Macular Degeneration showed this 60 percentage of individuals showed much better in visible acuity following combining micro present-day stimulation therapy and natural supplementation.

Drs. Leeway Halloran plus August L. Viewer studied 25 individuals declared with generally untreatable vision diseases including macular weakening, retinitis pigmentosa, CMV-retinitis, plus diabetic retinopathy. The individuals were handled with combining micro present-day stimulation therapy and natural supplementation. Overall final results showed outstanding increase with visual job in visible acuity in many and plainly established your safety with the combination of MCS therapy and natural supplementation.

Sustained-release implants on track for retinal vascular disease treatment

2011-01-23T10:56:00.000-08:00

by:Elias Reichel

KAANAPALI, Hawaii — Sustained-release corticosteroids will play a significant role in retinal vascular disease, but the current implants still need improvements, one presenter here said.

"It is important to realize [steroids] will have a continued role in our treatment of diseases. They may also serve for adjunctive [therapies] like stem cell treatments and [instances] where transplantation or immunoreactions may occur," Elias Reichel, MD, who discussed outcomes using Ozurdex (dexamethasone intravitreal implant, Allergan) and Iluvien (fluocinolone acetonide intravitreal implant, Alimera), said at Retina 2011. "So, having a better delivery system for corticosteroids is very useful for many of the diseases we are seeing in our offices."

Challenges include needing to achieve and maintain clinically effective concentrations in the vitreous over time while maximizing efficacy and minimizing adverse effects, Dr. Reichel said.

As part of a 6-month study, the dexamethasone implant demonstrated 2- to 3-month peak efficacy, had a low incidence of IOP issues and conferred a cataract progression of approximately 5%. Additionally, 45% of the patients gained three lines of visual acuity, Dr. Reichel said.

The U.S. Food and Drug Administration has approved the device for all retinal venous obstructive disease.

The fluocinolone implant is now part of a 36-month study and has demonstrated efficacy to at least 30 months. Between 30% and 40% of patients gained at least three lines of visual acuity. However, the device has a moderately higher risk of IOP issues and a cataract progression rate of 50%, according to Dr. Reichel.

The device has received a complete response letter from the FDA.

"Current formulations that we have are good but can be better," Dr. Reichel said. "We really have to look at longer duration and this reduced risk trade-off."

* Disclosure: Dr. Reichel is a consultant to Alimera and Allergan.

Stem cell therapy for macular degeneration

2011-01-15T01:31:00.000-08:00

By Jill U. Adams, Special to the Los Angeles Times

The FDA has approved a new study aimed at fighting dry age-related macular degeneration.

About 10 million Americans suffer some degree of vision loss caused by age-related macular degeneration, and that figure is expected to grow as more baby boomers become senior citizens. There is no cure for the disease, but last week the U.S. Food and Drug Administration gave a green light to an unusual clinical trial that seeks to restore patients' sight by employing human embryonic stem cells.

None of the stem cells will be injected into patients; instead, they are grown into another kind of cell that will be delivered to the back of the eye, where the retina is damaged by the disease. The hope is that the cells will help repair the damaged retinal tissue.

The company behind the trial, Santa Monica-based Advanced Cell Technology Inc., developed the therapy to treat Stargardt's macular dystrophy, a rare childhood version of macular degeneration that affects about 1 in 10,000 kids. The FDA gave the company permission to test the therapy in Stargardt's patients in November. However, if they work, the cells would have a much bigger effect as a treatment for age-related macular degeneration.

Here's a closer look at the disease and the new therapy.

What is age-related macular degeneration?

Age-related macular degeneration is the leading cause of vision impairment and blindness among people who are 65 and older, says Dr. Jose Pulido, an ophthalmologist at the Mayo Clinic in Rochester, Minn. The dry version of the disease begins with tiny deposits of fat and protein — called drusen — that appear in the center of the retina, called the macula. As the deposits grow in number and size over the course of years, things begin to look blurry in the center of a person's field of vision. As the disease worsens, the blurriness may progress to a blind spot.

What causes it?

The main problem is that light-sensing cells in the macula, called photoreceptors, slowly break down. This is thought to be caused by the loss of another population of cells, called retinal pigment epithelial (RPE) cells, which support the photoreceptors in a number of ways.

Among other things, the RPE cells release growth factors important for photoreceptors to thrive. "The RPE are also the garbage trucks of the retina," removing toxic byproducts that the retina makes as it performs its light-sensing function, says Stephen Rose, chief research officer for the Foundation Fighting Blindness, a fundraising organization based in Columbia, Md.

Dry age-related macular degeneration can also progress into wet age-related macular degeneration, in which blood vessels grow abnormally and leak fluid into the macula. It's a much more aggressive form of the disease, but it's also more treatable.

How can human embryonic stem cells help?

The stem cells are grown into healthy replacement RPE cells and injected into the retina, says Gary Rabin, Advanced Cell Technology's chief executive. The company hopes the lab-grown cells will replace the dying RPE cells and keep vision intact — or even restore it to some degree.

"We've had incredible success with this in animal studies," Rabin says. A study published in the journal Stem Cells found that the RPE cells restored eye function in sick mice and rats to "near-normal levels," and another study in Cloning and Stem Cells reported that the treatment improved vision in affected rats until it was 70% as good as that of healthy animals.

Of course, success in animal studies doesn't always translate to humans. In addition, the eyes of people in their 50s and 60s likely present "a very different milieu for the RPE cells to try to hook onto," Pulido says.

Rose adds that the treatment, if it works, wouldn't amount to a cure because it doesn't address the reason why RPE cells deteriorate in the first place. But it would buy time for patients, delaying vision loss for perhaps years. "That's huge," he says.

What will the new trial assess?

The FDA granted permission to conduct a Phase I/II clinical trial, which is essentially a safety trial, that will involve a dozen patients. The first patients will get a very low "dose" of cells — 50,000 — and will be monitored for any untoward effects.

"If there are no safety issues after three-ish months, we will increase the dose [to a level where we] hope to see efficacy," Rabin says. "We anticipate that the photoreceptor cells will awaken and that there will be a gradual increase in visual acuity over time." For now, the protocol calls for a one-time treatment of up to 200,000 cells.

Aren't there ethical concerns about using human embryonic stem cells?

Generally speaking, many people are troubled by research involving human embryonic stem cells because they are typically made by dismantling — and thus destroying — embryos that are a few days old.

Advanced Cell Technology uses a proprietary technique to extract a single cell from a young embryo, allowing the rest to remain intact and develop normally, Rabin says. A similar method is routinely used to biopsy embryos for pre-implantation genetic diagnosis, in which embryos created through in vitro fertilization are scanned for genetic disorders before being transferred to a uterus.

FDA approves embryonic stem cells to reverse macular degeneration

2011-01-09T01:39:00.000-08:00

by:Admin

Sacramento is now the hub of stem-cell research focusing on regenerative medicine. See the article, UC Davis: Stem Cell Research. After receiving $62 million for stem cell research last year, the new UC Davis Institute for Regenerative Cures opened. And the center already is testing dozens of therapies in the laboratory. The center will bring 200 scientists and laboratory personnel together under one roof. Check out the UC Davis Stem Cell Institute. See UC Davis Stem Cell Program. And check out the site, UCDMC Stem Cell Research News.

Now that the FDA has approved embryonic stem cells today, to help reverse certain types of macular degeneration, consumers should know that the stem cell taken from an embryo does not destroy the embryo. Just a single stem cell is taken from the embryo. Then the embryo continues to thrive and is not destroyed.

California sites currently under consideration for the trials include the Jules Stein Eye Institute at UCLA and the Ophthalmology Department at Stanford University. Check out the government site listing clinical trials, Clinical Trials.gov.
Also, in the Sacramento and Davis regional area, did you know that the University of California is recruiting for or has completed at least 193 clinical trials on various types of health studies ranging from the health benefits of ground flax seeds to stem cell research? Also see the January 4, 2011 news article, Read: Vitamin Drug Could Stop Dry Macular Degeneration.

Concerning studies at another university on macular degeneration and stem cell research, if you're interested in stem cell research for macular degeneration, the breaking news is that the FDA has just approved the use of stem cells to treat certain types of macular degeneration. According to a January 4, 2011 news article, "FDA Approves Stem Cell Treatment Trial for AMD-Related Vision Loss," the US Food and Drug Administration (FDA) has approved a clinical trial of human embryonic stem-cell treatments on patients who have suffered vision loss related to dry age-related macular degeneration (AMD).

Advanced Cell Technology of Massachusetts will begin a Phase I/II open-label study on twelve patients at multiple clinical sites to determine the safety and tolerability of the treatment. The dry version of macular degeneration is a leading cause of blindness in older adults. Dry age-related macular degeneration is one of two forms of an eye disease that breaks down retinal pigment epithelial (RPE) cells in the macula of the retina, a layer of light-sensitive tissue at the back of the eye. Progressive loss of RPE cells and the accompanying loss of photoreceptors can cause severe vision loss. There are no current treatments available for AMD.

Dry AMD is the leading cause of blindness in individuals over the age of 55, afflicting approximately 10 million people in the US. And as the population ages, according to the article, "FDA Approves Stem Cell Treatment Trial for AMD-Related Vision Loss."

In the clinical trials and approved experiments, patients will receive 50,000 to 2,000,000 RPE cells derived from human embryonic stem cells to replace those lost due to AMD. While human embryonic stem cell use is controversial, ACT maintains that their cells are derived from a single-cell extraction technology that “does not destroy the embryo.” Also read the article, Read: Smoking Raises Risk of Macular Degeneration.

Genetic Testing for AMD is here Today

2011-01-02T16:47:00.000-08:00

By; Diana Shechtman OD FAAO & Steven Ferrucci OD FAAO
Age-Related macular degeneration (AMD) is a progressive disease and the leading cause of vision loss among the elderly, affecting central vision required for daily activities such as driving and reading. There are a number of factors affecting AMD, such as advanced age, smoking, UV exposure, overall health (that contribute to high blood pressure, obesity, diet) and family history. Many factors may be modified and yet others like genetics cannot. Although AMD may seem to be hereditary in some families and not others, genetics have been shown to contribute significantly to the disease. Multiple twin and sibling studies have collaborated to the familial nature of the disease. First-degree relatives of patients with AMD are at a significantly increased risk for the disease. Furthermore, large epidemiological studies have suggested a strong genetic risk factor for AMD. In fact, the risk of developing AMD increases 4 fold among patients with a positive family history. In 2005 a breakthrough occurred in the area of genetic research and AMD; Klein and associates discovered a strong link between AMD and certain genetic variants. Similarly, numerous other genes have been implicated in AMD, which may increase the risk of AMD up to 70%.
Until recently there was no test to help determined patient’s inherited risk for AMD. Today, Macula Risk (ArcticDX, Toronto, Ontario) is a genetic test specifically designed to determine genetic predisposition to AMD and vision loss attributed to the more advanced stage of the disease.
Macula Risk  genetic test separates individuals into one of 5 macula risk (MR) categories, with MR 3 through 5 representing an increased risk for the more advance stage of the disease. This accounts for approximately 20% of the general population. MR1 has less than a 5% risk of the advanced stage of the disease, while MR 5 carries greater than 55% risk. These results can aid the doctor in devising a specific management plan and follow-up protocol in order to reassure early intervention to prevent vision loss.
The test only requires a simple in-office cheek swab, which is sent directly to the genetic lab. The report includes test results and written genetic support information (including access to genetic counseling). Macula Risk genetic testing is covered by most insurance providers, including Medicare, as long as the specific diagnosis (ICD-9) are identified by the doctor. The prognostic genetic test is intended for patients who have a diagnosis of early or intermediate AMD. Thus, the “at risk patient,” would have to pay a fee for the test.
Despite our best efforts and new treatment options available today, many people are still losing vision from AMD. New advancements in the area of AMD are becoming an integral part in preventing future visual deterioration. AMD is affected by both environmental and genetic factors that interact with one another to determine prevalence and progression of the disease. Furthermore, at this time we do not know all of the genes linked to AMD. Hence, genetic testing in the area of AMD is only a risk indicator and cannot predict “without a shadow of a doubt,” which patients will and which will not develop the disease. However, this test provides a genetic profile screening to help identify those at risk as well as aids in tailoring a distinct management approach for those with the disease. With various researches devoted to treatment options for AMD, genetic testing in the area of AMD is at the frontier of providing crucial information.
REFERENCES
1. Swaroop, Branham KE, Chen W, Abecasis G. Genetic susceptibility to age-related macular degeneration: a paradigm for dissecting complex disease traits. Hum Mol Genet 2007; 16: 174-82.
2. Klein ML, Mauldin WM, Stoumbos VD. Heredity and age-related macular degeneration. Observations in monozygotic twins. Arch Ophthalmol. 1994; 112: 932-7.
3. Meyers SM, Greene T, Gutman FA. A twin study of age-related macular degeneration. Am J Ophthalmol. 1995; 120: 757-66.
4. Heiba IM, Elston RC, Klein BE, et al. Sibling correlations and segregation analysis of age-related maculopathy: The Beaver Dam Eye Study. Genet Epidemiol. 1994; 11: 51-67.
5. Klaver CC, Wolfs RC, Assink JJ, et al. Genetic risk of age-related maculopathy. Population-based familial aggregation study. Arch Ophthalmol. 1998; 116: 1646-51.
6. Seddon JM, Ajani UA, Mitchell BD. Familial aggregation of age-related maculopathy. Am J Ophthalmol. 1997; 123: 199-206.
7. Klein RJ, Zeiss C, Chew EY, et al. Complement Factor H Polymorphism in Age-Related Macular Degeneration. Science 2005; 308: 385-389.
8. Seddon JM, Reynolds R, Maller J, Fagerness JA, Daly MJ, Rosner B. Prediction model for prevalence and incidence of advanced age-related macular degeneration based on genetic, demographic, and environmental variables. Invest Ophthalmol Vis Sci 2009; 50 (65): 2044-53.
9. www.macularisk.com/en/physicians/order.html (accessed Dec. 14th , 2010)

Zinc and Macular Degeneration

2010-12-27T05:52:00.000-08:00

By: Admin
Are you someone who has realized that they are suffering from age related macular degeneration?
Our sense of sight is something that is incredibly important to us, and the idea of having it threatened can be terrifying. The issue is that age related macular degeneration, often abbreviated to AMD is relatively common and after the age sixty, there is a thirty percent chance that this disorder can be developed and it is highly recommended that you use a antioxidant supplement as treatment/ therapy for macular degeneration.
The more research that you do into this condition and into the things that might have a hand in causing it, the more likely it is that you are going to see zinc listed as being something that can help this condition.

New Investment to Boost Gene Therapy Development

2010-12-20T05:54:00.000-08:00

National Neurovision Research Institute (NNRI), the Foundation Fighting Blindness’ clinical trial support organization, announced today that one of its key partners, biopharmaceutical company Oxford BioMedica, has established a collaboration with sanofi-aventis, a major international pharmaceutical company, to develop and commercialize gene therapy treatments for vision-robbing retinal degenerative diseases that affect tens of millions of people around the world.

The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; and RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries.

The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.

“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”

“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”

Based on the agreement, Oxford BioMedica will receive an upfront payment of $26 million and a further $24 million from sanofi-aventis over a three-year period.

The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina. For more information on this technology, visit www.oxfordbiomedica.co.uk/

German company's retinal implant can restore vision

2010-12-11T17:26:00.001-08:00

by: Retina Implant

Restoring vision to the blind is the sort of feat reserved for ancient religious texts and modern science fiction novels. But a company in Germany did just that with an eye implant.

Retina Implant AG is in the process of developing a sub-Retina Implant, designed to be inserted into the eye to treat back-of-the-eye disorders. A first clinical trial showed that the device can enable people suffering from a certain type of macular degeneration to see. The patients had retinitus pigmentosa, an inherited and incurable degenerative condition that causes tunnel vision and often, eventually, complete blindness. Retina Implant estimates that the condition affects about 200,000 people in the U.S. and Europe.

In 1995, the company’s founder and current board member Dr. Eberhart Zrenner said that implanting a chip inside the eye was as far-fetched as using the space shuttle to get to an adjacent star in the Milky Way. But Dr. Zrenner, who is also chairman of the University of Tuebingen Eye Hospital in Germany, didn’t give up. Ten years later the company launched its first human trial. At the time, Retina Implant also began talking to venture capital firms in Europe, but the technology was deemed too risky. It wasn’t until a wealthy businessman, who was personally interested because he had relatives who suffered from vision loss, that the company found significant outside investment.

Retina Implant isn’t the only group working on bionic-eye-like projects, but it seems to have a jump on the competition. Scientists at the Mass. Institute of Technology are also conducting clinical trials with their own version of a sub-Retina Implant, but don’t anticipate implanting their device in humans until 2013. Sylmar, Calif.-based Second Site Medical Products Inc. is developing a device for sufferers of retinitus pigmentosa, but that’s an epi-retinal prosthesis used in conjunction with an external camera attached to eyewear.

Retina Implant’s product sits underneath the retina ’directly replacing light receptors lost in macular degeneration,’ according to the company. Its most advanced and studied sub-Retina Implant is a 3mm-by-3mm microchip with an array of approximately 1,500 photosensitive electrodes. Electrical power for the device is provided inductively through transmitter coils attached to the skin.

In November, the company published results (PDF) from the first in-human clinical trial that proved the device can work in the Proceedings of the Royal Society B, a peer-reviewed academic journal. The company’s research with 11 human subjects showed that people who had been completely blind had regained up to two percent of their vision. enough to recognize letters in a newspaper headlines and see utensils before them when seated at a table. That number may seem insignificant ’ but it’s impossible to calculate the value a blind person places on seeing again, no matter how dimly.

In October, Retina Implant announced that it would increase its manufacturing footprint 25-fold (PDF).

Retina Implant is in the process of commencing a larger, 60-patient clinical trial in several sites across Europe. In this trial, the subjects will have the option to keep the implant permanently. In the first trial, the chips were all removed after four months except for one patient who lobbied the government to allow him to keep the device because his outcomes were so positive. To date, no complications have been reported, according to the company.

Retina Implant believes its device can win CE Mark approval in the European Union as soon as the end of 2011, but it does not have yet have definite plans for entering the U.S. market.

MassDevice recently spoke with Retina Implant CEO Walter Wrobel about the difficulties of developing such a technically advanced medical device and his company’s efforts to prove the device’s effectiveness enough to get it to market.

Drug Therapy To Cure Macular Degeneration

2010-12-06T06:36:00.000-08:00

By Administration

Lucentis-is a drug therapy based on the cancer drug Avastin for wet macular degeneration. The treatment involves periodic injection of the drug directly into the eye. A higher percentage of those treated with Lucentis have shown improved vision than with any other treatment. Macugen-is another drug therapy for macular degeneration. It also involves periodic injections directly into the eye. It employs a molecule that attacks a protein involved with the growth of macular degeneration related blood vessels. macular degeneration treatment Vitamins and Minerals-are a treatment that is being used to treat dry macular degeneration. There is evidence to suggest that vitamins and minerals that have antioxidant properties will slow the progression of intermediate dry macular degeneration to the advanced form. The treatment typically involves large doses of Vitamin C, Vitamin E, Beta Carotene and Zinc Oxide.
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Melatonin for Macular Degeneration?

2010-11-28T09:57:00.000-08:00

By Cathy Wong, Alternative Medicine Guide

Melatonin may help treat age-related macular degeneration, according to a recent report. A leading cause of blindness in the United States, age-related macular degeneration develops when certain cells in the retina deteriorate and gradually destroy your central vision.

A hormone with antioxidant effects, melatonin may help stop shortening of telomeres (chromosomal structures that become shorter over time due to factors like aging, inflammation, and damage caused by free radicals). By preventing telomere-shortening in the cells of the retina, the report suggests, melatonin may help preserve eyesight and slow the progression of age-related macular degeneration.

While melatonin shows promise as a natural remedy for age-related macular degeneration, it's too soon to recommend melatonin supplements for this condition. For help in protecting your eyesight as you age, wear UV-protective lenses when outdoors in the daylight and consider upping your intake of foods rich in lutein (such as leafy green vegetables, green beans, and mango).

As always please check with your doctor before starting/ or changing any medications or supplements.

Acceleron's ACE-041 Demonstrates Clinical Efficacy

2010-11-22T11:06:00.000-08:00

By Acceleron
CAMBRIDGE, Mass – November 19, 2010 – Acceleron Pharma, Inc., a biopharmaceutical company developing novel protein therapeutics that regulate the growth and development of tissues and cells, including muscle, bone, red blood cells, and vasculature, today announced the presentation of interim results from the first-in-human clinical study of ACE-041 in patients with advanced cancer at the 22nd EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Berlin, Germany. The presentation was given by Professor Sunil Sharma, the Jon and Karen Huntsman Presidential Professor of Cancer Research at the Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah.

“It has been very encouraging to see so many signals of efficacy in this trial, in particular because these are end-stage cancer patients,” said Dr. Sunil Sharma. “It is also important to note that while we have demonstrated significant activity with ACE-041 monotherapy in this study, we might expect to see even more efficacy in future studies with ACE-041 used in combination with other therapies.”

“The clinical activity and safety profile of ACE-041 confirms our understanding that the ALK1 pathway plays a fundamental and distinct role compared to the VEGF-axis in tumor angiogenesis,” said Dr. Matthew Sherman, M.D., Chief Medical Officer at Acceleron Pharma. “This has significant implications because nearly all patients treated with VEGF inhibitors eventually either fail therapy or develop resistance to these drugs. There is a tremendous need for novel therapies that go beyond VEGF to target the tumor blood supply.”

In a phase 1, first-in-human clinical study, patients with advanced-stage tumors were treated with multiple ascending doses of ACE-041, to evaluate the safety and pharmacokinetics of ACE-041. This study also explored antitumor activity of ACE-041.

Summary of interim findings presented:

· ACE-041 subcutaneously (SC) injected once every three weeks (q3w) is generally well-tolerated · Common side effects include mild or moderate peripheral edema, fatigue, nausea, headache, anorexia, and anemia. A single case of Grade 3 congestive heart failure was reported · Toxicities commonly associated with VEGF inhibition (hypertension, proteinuria, or bleeding) have not been observed · ACE-041 pharmacokinetics support dosing every 3 weeks · One patient with refractory head and neck cancer achieved a partial response and three patients had prolonged disease stabilization · Rapid reduction in tumor metabolic activity observed in several patients, measured by FDG-PET imaging · An expanded cohort study is ongoing at the dose level intended for Phase 2 studies,

ACE-041 is being developed for the treatment of advanced cancer and age-related macular degeneration (AMD).

About ACE-041

ACE-041 is a recombinant receptor fusion protein that inhibits angiogenesis by preventing BMP9 and BMP10, members of the TGFβ protein superfamily, from interacting with activin receptor-like kinase 1 (ALK1), a receptor that is found on proliferating endothelial cells. ACE-041 inhibits ALK1 signaling, which is required for the development of mature, functional capillary networks. In animal studies, treatment with ACE-041 inhibits tumor angiogenesis and growth and ocular neoangiogenesis. In a clinical study of patients with advanced, refractory solid tumors, treatment with ACE-041 was generally well-tolerated and antitumor activity was observed, resulting in tumor shrinkage and stabilization of disease. ACE-041 is being developed for the treatment of advanced-stage cancer and age-related macular degeneration (AMD).

About Acceleron Pharma

Acceleron is a privately-held biopharmaceutical company committed to discover, develop, manufacture and commercialize novel biotherapeutics that modulate the growth of red blood cells, bone, muscle, fat and the vasculature to treat musculoskeletal, metabolic and cancer-related diseases. Acceleron’s scientific approach takes advantage of its unique insight into the regenerative powers of the TGF-β superfamily of proteins. Acceleron utilizes proven biotherapeutic technologies and capitalizes on the company’s internal GMP manufacturing capability to rapidly and efficiently advance its therapeutic programs. The investors in Acceleron include Advanced Technology Ventures, Alkermes, Bessemer Ventures, Celgene, Flagship Ventures, MPM BioEquities, OrbiMed Advisors, Polaris Ventures, QVT Financial, Sutter Hill Ventures and Venrock. For further information on Acceleron Pharma.

Macular Degeneration Treatments/Therapies Breakthroughs

2010-11-15T19:44:00.000-08:00

by Isobel Washington

Macular degeneration is an eye condition characterized by the deterioration of the macula, which is the central "lens-like" part of the eye's retina responsible for sharp central vision. Affecting central vision and often leading to vision loss, macular degeneration has had limited treatment options. Recently, there have been some breakthroughs to help patients retain vision.

Significance
Macular degeneration is the leading cause of vision loss and blindness among Americans age 65 and older. Vision loss from this condition is a growing problem, since this age demographic represents an increasingly larger percentage of the U. S. population.

Function
Treatments for macular degeneration work to preserve vision ability at the time of treatment, and slow the progression of the disease (it's a progressive disease that affects vision over time). Treatment cannot restore vision that is already lost through the disease. There is no cure or treatment to stop the progression of macular degeneration, there are ways to preserve and prolong current vision.

Eye Injections
Lucentis and Macugen are FDA-approved ocular injection treatments, and are highly effective for preserving vision and inhibiting macular degeneration symptoms, according to AllAboutVision.com. A 2005 study on Lucentis demonstrated success rate of 95 percent for improving and sustaining vision in macular degeneration patients.

Laser Treatment
Laser technology is now used to destroy the abnormal, leaky blood vessels that cause vision loss in macular degeneration patients. The National Eye Institute points out, however, that while this treatment may be effective for preventing vision loss, it is also comes with the risk of destroying healthy tissue that surrounds the treatment area.

Photodynamic Therapy
This method uses special light treatment to activate an injected drug, verteporfin, in the blood vessels, so that it destroys the new, abnormal blood vessels being hyper-produced in the eye (those that cause vision impairment or loss). The National Eye Institute reports that this light-activation method slows vision loss, but doesn't stop it.

Investigational Treatments
Investigational treatments for macular degeneration, in various stages of research and FDA clinical studies, include Avastin, a cancer treatment drug. As of 2009, the National Eye Institute reports that no available treatment provides a cure for macular degeneration, and that vision loss may result, despite treatment.

About the Author
Isobel Washington has been a freelance journalist since 2007. Washington's work first surfaced in Europe, where she served as a restaurant critic and journalist for "LifeStyles" magazine. Her love of travel and culture inspired her first novel, which is currently underway. Washington has a 10-year career in marketing communication and holds a Bachelor of Science degree.

Qualifing Theraputic Discovery Project Program

2010-11-04T05:50:00.000-07:00

by GEN news

Over the last couple of days, companies have been reporting on awards received under the Qualifying Therapeutic Discovery Project program. The IRS in conjunction with the Department of Health and Human Services, approved applications for projects that showed significant potential to produce new and cost-saving therapies, support jobs, and increase U.S. competitiveness.

Under the program, a total amount of $1 billion was allocated for credits and grants with a $5 million limit per each eligible applicant. The full list of companies receiving these awards can be found at http://bit.ly/b3VxSp.

Here are details for a few more companies:

Acceleron Pharma received five grants totaling $1,222,396.25: ACE-031 for Duchenne muscular dystrophy, ACE-536 for myelodysplastic syndrome, ACE-435, ACE-011 for anemia, and ACE-041 for advanced solid tumors, multiple myeloma, and age-related macular degeneration.

Aestus Therapeutics received one grant of $244,000: chronic neuropathic pain drug development.

BioCryst Pharmaceuticals received five grants totaling $1,064,297.89: four grants of $244,479.25 each were given to peramivir for influenza, BCX4208 for gout, forodesine for CLL and CTCL, and JAK inhibitor programs in psoriasis, ankylosing spondylitis, and multiple sclerosis. One grant of $86,380.89 was awarded to BCX4161 for hereditary angiodema.

Biodel received five grants totaling $1,222,396.25: Linjeta, VIAtab, smart basal, glucagon, and glargine.

Cardium Therapeutics received one grant of $244,479.25: Generx for advanced coronary artery disease.

Celsion received one grant of $244,479.25: Thermodox for primary liver cancer and recurrent chest wall breast cancer.

Cerus received two grants totaling $488,958.50: Intercept Blood System for platelets and red blood cells.

Charleston Laboratories received one grant of $244,479.25: CL-108 for moderate-to-severe pain.

CorMedix received two grants totaling $488,959.50: Neutrolin and Deferiprone.

Curis received two grants totaling $488,958.50: CUDC-101 and pipeline small molecules for cancer treatment.

Derma Sciences received one grant of $244,479.25: DSC127 for tissue repair.

Dicerna Pharmaceuticals received two grants totaling $488,958.50: Dicer Substrate Technology and DsiRNA molecules for the treatment of cancer.

DNA Medicine Institute received a grant of $222,999: Universal Blood Sensor.

Enzon Pharmaceuticals received five grants totaling $1,222,396.25: PEG-SN38, mRNA antagonist for HIF-1 alpha, Survivin, Androgen Receptor, and HER3.

Etubics received one grant of $244,479.25: CEA-expressing adenovirus as a colon cancer therapeutic vaccine.

GTx received five grants totaling $1,222,396.25: ALK inhibition therapy, Toremifene 20 mg, Ostarine, GTx-758, Toremifene 80 mg, which are all being developed for cancer and cancer supportive care.

Health Discovery received a grant of $244,479.25: SVM and RFE-SVM technology.

Icagen received three grants totaling $733,000: Selective sodium channel drugs to treat chronic pain, KCNQ agonists for epilepsy and pain, and TRPA1 drugs for inflammatory pain.

Inviragen received two grants totaling $488,958.50: Vaccines against dengue and chikungunya viruses.

InVivo Therapeutics received a grant of $244,000: biocompatible polymer scaffolding device designed for implantation into a lesion to treat acute open-wound SCI.

Light Sciences Oncology received two grants totaling $488,958.50: Aptocine for treatment of primary and secondary liver tumors and benign prostatic hyperplasia.

Lipocine received four grants totaling $977,917: hormone replacement therapy, high-risk pregnancy support, oral treatment of progressive glioblastoma multiforme, and opioid-resistant cough in advanced cancer patients.

Molecular Detection received a grant of $244,479.25: Detect-Ready panel that detects carriers of MRSA and related pathogens.

Neoprobe received a grant of $244,479.25: Lymphoseek.

Omeros received eight grants of uneven amounts totaling $1,723,086.51: PDE7 for Parkinson disease; addiction treatment; therapies for osteoarthritis and the protection of articular cartilage; drugs to treat pain, inflammation, and spasm of the urinary tract; MASP-2 MoAb for traumatic injury; medications for schizophrenia; intracameral OMS302 to maintain intraoperative mydriasis and reduce pain and inflammation; and products to improve function and reduce pain after arthroscopic surgery.

OncoMed Pharmaceuticals received five grants totaling $1,222,396.25: OMP-21M18, OMP-59R5, novel antibodies, Wnt pathway inhibitors, and drugs targeting the Wnt pathway in cancer stem cells, all for the treatment of cancer.

PolyMedix received two cash grants totaling $488,958.50: PMX-30063 for acute bacterial skin and skin structure infections (ABSSSI) caused by Staph and PMX-60056 in percutaneous coronary intervention patients.

pSivida received two cash grants totaling $488,958.50: research on new generations of the company’s drug delivery technologies targeting ophthalmic diseases.

Quanterix received three grants totaling $733,437.75: Diagnostics developed on the Single Molecule Array (SiMoA) for prostate cancer, Alzheimer disease, and Crohn disease.

Regulus Therapeutics received two cash grants totaling $488,958.50: miRNA therapeutics for HCV and fibrosis.

Sangamo BioSciences received four grants totaling $977,917: SB-509 for diabetic peripheral neuropathy, SB-509 for amyotrophic lateral sclerosis, SB-728-T for human immunodeficiency virus/acquired immunodeficiency syndrome, and SB-313-xTZ for recurrent or refractory glioblastoma multiforme.

Sea Lane Biotechnologies received six grants totaling $1.5 million: Surrobody™ therapeutic candidates and influenza antibodies.

Soligenix received a grant of $244,479.25: orBec in acute gastrointestinal graft vs. host disease.

Somaxon Pharmaceuticals received a grant of $244,479.25: Silenor.

Spectrum Pharmaceuticals received four grants totaling $977,917: RenaZorb for hyperphosphatemia in patients with chronic kidney disease and anticancer agents Zevalin, Apaziquone, and Belinostat.

Spherix received two grants totaling $469,478.50: triglycerides.

StemCells received four grants totaling $977,917: HuCNS-SC for diseases and disorders affecting the brain, the spinal cord, and the eye as well as hLEC human liver engrafting cells.

Synergenz BioScience received one grant of $94,836: Respiragene, a genetic-based test for lung cancer predisposition.

Telik received five grants totaling $1,222,396.25: Telintra in severe chronic neutropenia, Telcyta for refractory lymphoma and multiple myeloma, Telintra in low-to-intermediate-1 risk myelodysplastic syndrome, Telintra and Revlimid in myelodysplastic syndrome, and aurora and VEGFR kinase inhibitors for the treatment of cancer.

Threshold Pharmaceuticals received two grants totaling $488,958.50: TH-302 for the treatment of cancer, and the company’s hypoxia-activated prodrug technology platform for drug discovery.

Xoft received two grants totaling $469,478.50: electronic brachytherapy for the treatment of breast cancer and gynecological cancers.

Zalicus receive a grant of $244,479.25: Synavive for immunoinflammatory diseases.

Ziopharm Oncology received three grants totaling $733,437.75: Indibulin, Palifosfamide, and Darinaparsin, all for the treatment of cancer.

Retinal Disease Highlights From the 2010 AAO Meeting

2010-10-30T13:33:00.000-07:00

By Dr. Randall Wong

Many of us just returned from the largest ophthalmic “trade show” in the world. The American Academy of Ophthalmology convened in Chicago last week. This meeting was combined with the Middle East Africa Council of Ophthalmology (MEACO). Perhaps 40 K attended the meeting.

I also attended the 2 day retinal subspecialty meeting which preceded the larger AAO meeting. Thus, I had 5 days to expand my knowledge.

Most of the congress was focused on technology, especially electronic medical records. Few discoveries were revealed. This may be for two reasons: there is nothing really new going on right now, and/or, the Internet allows such rapid sharing of information, that it is impossible to “wow” anyone at this meeting. Probably both are true.

With regard to retinal disease, my particular specialty, there is little new, but lots to be excited about.

Avastin and Lucentis continue to be the mainstays of treatment for wet macular degeneration. There is evidence that the two drugs are similar in clinical efficacy…a notion I support. It is likely that these types of drugs will be delivered with a sustained release system, thus, obviating the need for repeated intraocular injections.

Ozurdex is now indicated for the treatment of uveitis. It was originally FDA approved for the treatment of RVO only. By itself, not earth-shattering, but does make sense clinically. Sustained release steroids for chronic intraocular inflammation. Sounds much better.

The highlight of the meeting is the potential for Iluvien to be FDA approved soon. Iluvien is similar to Ozurdex in that both are injectable intraocular sustained release systems. Iluvien will be a sustained release system that delivers intraocular steroids for the treatment of diabetic macular edema. While this is a particularly promising development for patients with diabetic retinopathy, this has larger implications for eye treatment overall.

What Does This Mean? Illuvien is likely to be the second FDA approved intraocular drug delivery system. This will be a significant endorsement of drug delivery to the eye. We are entering a new era of pharmaceutical therapeutics; sustained release inside the eye. For now, we are focused on retinal disease. But soon, very soon, devices will emerge promising better therapeutics for almost any eye condition.

Just think, glaucoma may be treated by such a device.

Novartis therapy Lucentis recommended for approval in EU to treat Diabetic Macular Edema

2010-10-23T19:34:00.000-07:00

By Thomas Reuters
- CHMP positive opinion supports Lucentis approval in EU for treatment in patients with visual impairment due to diabetic macular edema (DME)

- Pivotal data shows Lucentis provided rapid, superior and sustained vision gains compared to the current standard of care

- Diabetes-associated eye diseases such as DME are a leading cause of blindness in most developed countries in the working-age population

Basel, October 22, 2010 - Novartis has received a positive opinion from the Committee for Medicinal Products for Human Use (CHMP) for Lucentis(R) (ranibizumab) for the treatment of patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.

"Lucentis was designed specifically for use in the eye, and its efficacy and safety have now been demonstrated in patients suffering loss of vision due to diabetic macular edema through a robust program of clinical trials," said David Epstein, Division Head of Novartis Pharmaceuticals.

The submission was supported by data from two Novartis-funded clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy therapy) or laser therapy, the current standard of care. The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy achieved an average 5.9 letters and 5.5 letters gain in visual acuity at 12 months, respectively, compared to laser-treated patients as measured on a standard ETDRS eye chart.

The RESOLVE study showed that Lucentis-treated patients achieved an average 11.7 letters gain in visual acuity at 12 months compared to sham-treated patients, some of whom received laser treatment.

The pivotal data from RESTORE and RESOLVE are further supported by results of an independent US study conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), showing that at one year nearly 50% of patients' eyes treated with Lucentis and laser therapy improved their visual acuity by 10 letters or more, compared to 28% with laser alone. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years.

Lucentis was generally well tolerated in clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with that previously reported in large controlled clinical trials, and in rigorous monitoring since Lucentis was first approved for wet age-related macular degeneration (AMD). Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD.

Diabetic macular edema (DME) is a consequence of diabetic retinopathy - the most common diabetic eye complication, characterized by changes in the blood vessels of the retina - to the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.

Lucentis offers an entirely new pharmacological approach to treatment compared to the current standard of care for DME that involves the use of laser burns to stop the capillary leakage and to reduce swelling. Lucentis is an antibody fragment that is injected into the eye and acts by neutralizing vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.

Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema. The results are expected in 2011. Novartis has exclusive rights in the rest of the world and plans to file in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema following RVO.

Disclaimer

The foregoing release contains forward-looking statements that can be identified by terminology such as "recommended," "plans," or similar expressions, or by express or implied discussions regarding potential new indications or labeling for Lucentis or regarding potential future revenues from Lucentis. You should not place undue reliance on these statements. Such forward-looking statements reflect the current views of management regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results with Lucentis to be materially different from any future results, performance or achievements expressed or implied by such statements. There can be no guarantee that Lucentis will be submitted or approved for any additional indications or labeling in any market. Nor can there be any guarantee that Lucentis will achieve any particular levels of revenue in the future. In particular, management's expectations regarding Lucentis could be affected by, among other things, unexpected clinical trial results, including unexpected new clinical data and unexpected additional analysis of existing clinical data; unexpected regulatory actions or delays or government regulation generally; competition in general; government, industry and general public pricing pressures; the company's ability to obtain or maintain patent or other proprietary intellectual property protection; the impact that the foregoing factors could have on the values attributed to the Novartis Group's assets and liabilities as recorded in the Group's consolidated balance sheet, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

Complement inhibition may be the future of dry AMD therapy

2010-10-17T13:34:00.000-07:00

CHICAGO — Ongoing clinical trials exploring the use of complement inhibitors for treating nonexudative age-related macular degeneration offer promise for a disease state that has long been considered difficult to treat.

A number of recent studies have implicated the complement immune system in AMD. However, nonexudative AMD remains a "uniquely human disease," and, therefore, no animal model exists in which to prove potential therapeutic strategies, Philip J. Rosenfeld, MD, PhD, said here are Retina Subspecialty day preceding the joint meeting of the American Academy of Ophthalmology and the Middle East Africa Council of Ophthalmology.

As a result, Dr. Rosenfeld said, human trials will prove important in determining whether complement inhibition is of any real clinical benefit.

Several such trials are already underway. Alcon is currently investigating its POT-4 (AL-78898A) anti-C3 cyclic peptide in human trials. There is some evidence that POT-4 may also affect VEGF expression in the retina, Dr. Rosenfeld said.

Separately, Genetech/Roche has an anti-factor D (FCFD4514S) that inhibits the C3 and C5 alternative pathway convertases. Phase 1 studies have been successfully completed with that agent, Dr. Rosenfeld said.

Two separate C5 inhibitors are being studied: Eculizumab/Sollris (Alexion) and ARC1905, an anti-C5 aptamer (Ophthotech).

"One of the advantages is that while you block the downstream activated species, you preserve the more proximal species that are important for the clearance of bacteria, particularly the encapsulated organisms," Dr. Rosenfeld said.
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Angiogenesis Discovery Points to Novel Therapy for Multiple Diseases

2010-10-10T06:12:00.000-07:00

Tatiana Byzova, PhD, a faculty member in Lerner Research Institute's Department of Molecular Cardiology and Director of the Center for Angiogenesis Research, and colleagues have discovered a fundamental biological pathway in angiogenesis (formation of blood vessels), published online October 3, 2010 in Nature (DOI: 10.1038/nature09421). The significance of this discovery is summarized by Dr. Byzova, in that "it affects many biological processes - from wound healing to aging."

Some pathologies included in that spectrum are age-related macular degeneration, atherosclerosis, and rheumatoid arthritis, while their published data indicate a particularly notable role in cancer. The results of this advanced understanding point to an exciting new approach for novel therapies.

In 1989, a protein called vascular endothelial growth factor (VEGF) was identified as a trigger of angiogenesis. This discovery led Genentech to develop the first effective treatment for macular degeneration; related work contributed to the development of a drug to block VEGF function in cancer, essentially starving the tumor of the nutrients the blood would otherwise bring.

However, although many tumors respond to anti-VEGF treatment, most develop resistance to the therapy and continue to survive over time. One possible explanation is that VEGF is not the only trigger leading to angiogenesis. This is precisely what Dr. Byzova's team has found.

Dr. Byzova's research has identified a class of oxidized lipids that are abundantly present in highly vasculated tumors. Further interrogation parsed out the process through which these products induce new blood vessel formation. It appears that cells use a family of receptors previously known to recognize foreign products such as bacteria to sense and respond to the danger of oxidation. The results point to a novel therapy that may well be an alternate way to starve the tumors that have managed to survive despite VEGF inhibition. Through uncovering a potential way to get around tumor resistance to VEGF, Dr. Byzova's group has opened up new doors for developing treatments for cancer. The fundamental discovery also provides substantial insight for novel treatments for other diseases that involve inflammation, oxidative stress, and angiogenesis.

Overall, this foundational discovery of a novel mechanism of angiogenesis comes just one year after Dr. Byzova headed a study that pioneered the identification of a new genetic-based human disease, published in Nature Medicine.

Retinal Degeneration Can be Prevented with Nanotechnology Gene Therapy

2010-10-04T09:00:00.000-07:00

Friday, 01 October 2010

Researchers from Tufts University published results from a study showing vision-saving gene therapy to the eyes can be delivered via nanotechnology. A protein called Glial Cell Line-Derived Neurtrophic Factor (GDNF) can protect the eyes from diseases of the retina, such as and retinitis pigmentosa.
The previous method for delivering genetic material with a virus had several problems and side effects. Although the study is in its infancy, and the results are temporary, mice injected with the GDNF carrying nanoparticle had a 3.9 to 7.7-fold reduction in damage to the retina. Seven days after treatment, the GDNF-nanoparticle treated mice had up to 39% better eyesight than mice in the control group.
Two weeks after the treatment, GDNF-nanoparticle-injected mice had nuclear layers of the retina that were almost 24 to over 39 percent thicker than control mice. However, after 14 days, these advantages seem to have vanished. According to Dr. Brett Katzen, "The idea of using gene therapy to help cure - or at least improve - the eyesight of patients with macular degeneration should be exciting to eye doctors everywhere. This is a great first step." The research shows an incredible potential for nanotechnology to develop an effective carrier for delivering gene therapy.
This therapy can then lead to a new generation of treatments for retinal diseases. Age-related macular degeneration is the leading cause of blindness in Americans over the age of 65.

Glaucoma eye drops showing some effect against Macular Degeneration

2010-09-18T01:29:00.000-07:00

by Dr. Edward Paul

Eye redness was the clue that something was happening to Celia Ramirez's vision. Although she wasn't having trouble driving or doing other tasks, her children urged her to have a checkup. It turned out she was in the early stages of age-related macular degeneration (AMD), a disease that attacks a person's central field of vision.

Mrs. Ramirez, who lives in the Rio Grande Valley, had surgery that successfully controlled her eye pressure, but her central vision continued to degrade.Eye specialist William Sponsel, Ph.D., associate professor and director of research at the Department of Ophthalmology at the University of Texas Health Science Center at San Antonio (UTHSC).Found a treatment with a new combination of drugs.

The miracle is the carbon dioxide, which is crucial for vision. The healthy eye produces enough carbon dioxide to dilate blood vessels around the retina and maintain proper blood flow. The ailing eye does not produce enough. This holds important implications for the treatment of patients with blinding eye diseases such as AMD and glaucoma, which are marked by diminished circulation of blood in the back of the eye. Eye pressure also is a conventional barometer of eye health.

About 60 of 65 patients have seen their vision improve while receiving treatment at UTHSC's teaching hospital, University Hospital. "The patients are receiving combination drug therapy, including agents that trick the eye into retaining more of its carbon dioxide," Dr. Sponsel said. "We have patients with glaucoma and no AMD, patients with AMD and no glaucoma, and patients with both disorders. All appear to demonstrate benefit in the central visual area, regardless of the cause of that visual loss."

The Health Science Center is the first medical center to initiate this combination therapy for patients with central visual loss, Dr. Sponsel said. Considerable research yielded the conclusions that now help patients. "You don't expect these patients to get better, you expect them to get worse," he said. "We have seen dramatic results that bode well for treatment of these disorders in the future."

The researchers measure patients' sensitivity to light on visual function tests. An increase of 10 points represents more than a million-fold increase in actual visual acuity. Mrs. Ramirez's vision in the macula -- the central visual area that enables perception of letters and colors -- was scored as virtually zero on early tests. After the recent treatment, her score is now 24.

The miracle agents are called "carbonic anhydrase inhibitors" (CAI's). Given as eye drops, CAI's reach the back of the eye rapidly and slow the clearance of carbon dioxide while increasing the supply of nutrients. They help dilate blood vessels within and behind the retina, which is the structure that receives, processes and transmits visual images relayed from the brain.

Dr. Sponsel pursued this line of research in an intriguing way -- after discovering that adults who hyperventilated and rapidly blew off their body's carbon dioxide showed decreased vision, eye pressure and circulation in the back of the eye. He was treating subjects one week with a CAI called dorzolamide and the next week with placebo eye drops. During hyperventilation, the subjects on dorzolamide maintained good light sensitivity in their central field of vision, while the same subjects during placebo treatment showed central visual loss. Dr. Sponsel holds two U.S. patents on this work. One valuable aspect of the research is that it proves increased eye pressure is not necessarily the definitive indicator of eye vessel disease.

Macular Degeneration and your eyesight

2010-09-13T06:52:00.000-07:00

You have most probably heard of this very common condition that damages your eyesight as you age. Because this condition affects more elderly people it is often referred to as age-related macular degeneration. Unfortunately there is no cure available for this condition however there are treatments that can help. This blog outlines the latest in research and treatments regarding macular degeneration and aims to help you make the most out of your eyesight in the mean time.

Now macular degeneration as the name implies affects the macula, which is an area right at the back of the eye on a structure that detects light known as the retina. Your macula is the part of the retina that allows you to see things in great detail. In fact many birds have better maculas than us, as they need to see things in great detail from up in the air. The condition of macula degeneration implies that the macula is damaged and as this damage becomes more extensive your eyesight will be affected. There are two types of macula degeneration and they are known as the wet or the dry type, the most common of the two is ‘dry’ maculae degeneration. In this type you get little yellow patches that pop up around your macula and your vision slowly worsens. In ‘wet’ macula degeneration there are tiny blood vessels in the back of your eye that grow and then leak out blood and other fluid. This tends to make ones vision worse more quickly and you should note that dry degeneration can turn into the wet kind.

Those who present with this condition for the most part have difficulty reading, making out fine detail and even have trouble recognizing friends and families faces. After a few years of having this condition things that are in the middle of your vision will begin to look blurred and you may struggle to make things out. After a while the middle of your vision may just appear black and you often cant see anything in this area, this means that you will be unable to see things that are right in front of you. However your peripheral vision will not be affected.

There are things that you can do to cope with this condition as well as medicines that can help. Your doctor may teach you how to make better use of your peripheral vision and tell you that using bright lighting in your home will help you see better. You may also need to make text on the computer screen bigger and use magnifying glasses when reading a book. Most of the medical treatments are aimed at the treatment of wet macular degeneration and in fact there are not many effective treatments for the dry variety. Laser therapy can be used to stop the macular degeneration from getting worse in the sense that these lasers burn away those yellow patches that form around the macular early in the disease course. Also there is no need to worry as laser therapy is not painful and is quite quick, however the evidence supporting this form of treatment is not great at this stage. In fact some research suggests that laser treatment can cause new blood vessels to from on the back of the eye that can make your sight worse.

Mineral and vitamin supplements may be useful in slowing down or stopping macula degeneration from occurring. You should take zinc, vitamin E and C as well as beta-carotene. Remember here that you will need to take them for a long time and in high doses to be affective and remember that these are not without their side effects. Some people find that they have problems with passing urine, others complain of stomach pains and some people notice that their skin turns a little yellow. If this is that case with you then you should stop taking the tablets and visit your doctor.

Wet macular degeneration can be treated with photodynamic laser surgery whereby a dye that is sensitive to light is injected into your bloodstream and then a laser is shone into your eye. The dye that was injected into the blood helps the laser to destroy all of those leaky blood vessels that are damaging your eye. This method has mixed reviews on effectiveness and one should have a good discussion with their doctor regarding the risks and benefits of this procedure before having it done.

There is another type of laser that can be used to destroy the blood vessels in the eye that leak, but this is only affective in a few people with very severe disease. There is a chance with this procedure that the blood vessels will grow back anyway and the laser can sometimes damage the eye. Radiotherapy is another option but lacks suitable research to say whether or not it works and we always worry that radiation may damage other parts of the eye.

There is an injection that you can have in your eyeball called pegaptanib, however for obvious reasons not many people like the idea of this if they can help it. Also you have to have two injections every month and the evidence is not great that it works wonders, although there are some convincing studies. There is another injection called ranibizumab that you get in your eyeball and this also does not have great results but is indicated in people with wet macular degeneration that is getting worse.

So the most important thing is what will happen to you and in this case the outcome is not fantastic. Over many years your vision will gradually get worse and it will be much worse in the centre of your vision than in the peripheries and you are unlikely to go completely blind. Unfortunately we don’t know how quickly things will turn bad and each patient is different, but most people manage to get around even with severe disease as they are able to use their peripheral vision much more effectively.

FDA grants pSivida, Alimera expedited review for macular degeneration therapy

2010-09-01T18:47:00.000-07:00

FDA grants pSivida, Alimera expedited review for macular degeneration therapy
August 31, 2010 by MassDevice staff

pSivida Corp. and Alimera Sciences win priority review status for their Iluvien drug/device combination, designed to treat diabetic macular degeneration.
PSDV, ALIM logos

The Food & Drug Administration put pSivida Corp. (NSDQ:PSDV) and Alimera Sciences Inc. (NSDQ:ALIM) on the fast track, granting an expedited review for their drug/device combination designed to treat diabetic macular edema.

Watertown, Mass.-based pSivida and Alpharetta, Ga.-based Alimera filed a new drug application with the FDA in June for Iluvien, a sustained release drug delivery system that delivers flucocinolone acetonide, a steroid, for the treatment of DME.

The federal watchdog agency granted priority review status to the application, moving the goal for finishing the review from 10 months back to six months.

That means a response could drop during the fourth quarter, pSivida president and CEO Dr. Paul Ashton said in prepared remarks, adding that FDA approval would trigger a $25 million milestone payment from Alimera.

The milestone payment wouldn't be the first time Alimera ponied up for pSivida. Its $72 million IPO in April triggered the repayment of a $15 million loan and $225,000 in interest. The companies are seeking European approval for Iluvien. If it makes it to market, pSivida will collect 20 percent of the net profits.

The FDA has already cleared a pair of pSivida products: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc. The company is also developing other ophthalmic products with Pfizer Inc. (NYSE:PFE), its largest shareholder, and has products of its own in the pipeline outside of ophthalmology, according to a press release.

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Gene therapy can correct inherited retinal eye diseases

2010-08-23T07:10:00.000-07:00

Researchers at the American Academy of Ophthalmology have found that Leber’s congenital Amaurosis (LCA), a very severe form of retinal disease
can be improved with the help of gene therapy.

Not only that, but the improvements were also found to be stable for two years.

Gene Therapy Can Correct Retinal Eye Diseases: LCA can be diagnosed in children at a very early age, sometimes even at infancy.

The main symptoms
of LCA are severity in vision loss and nystagmus(involuntary eye movement). By the time a person reaches his thirties or forties LCA develops into blindness.

* The impact of gene therapy could mainly be observed in children. The visual acuity and light sensitivity was tremendous in these children.
* Not only in children, researchers were also able to observe improvement in adults.

The Research and Theory: LCA is due to the mutations caused in any of the 13 genes in our body. Researchers were studying a Type 2 LCA which is due to mutation in the RPE65 gene.

* The doctors injected a normal functioning RPE65 gene which was joined with a virus into the sub-retinal space upon performing a surgery.
* The altered virus places the normally functioning RPE65 gene into the diseased cells and modifies the defective enzymes.
* After 2 weeks from the date of surgery, doctors observed that the patients reported an improvement in vision even in dim light.
* There were a few patients who also said that their visual acuity improved.
* A few even experienced massive improvement in nystagmus.
* The most encouraging result was that none of the patients experienced adverse effects.

Gene therapy does not improve sight on a permanent basis. But, gene therapy can correct inherited retinal eye diseases and help people restore sight.

People who undergo gene therapy need not be classified as blind any more. Researchers are trying hard to implement this technique in a safer way in younger children.

Drug Research could lead to AMD therapy

2010-08-18T07:47:00.000-07:00

By Adrian Galbreth

New drug research may pave the way for more effective treatments of age-related macular degeneration - the leading cause of blindness in the western world.

Those are the claims being made by researchers at Tufts University School of Medicine, who say that a protein known as galectin-3 promotes the growth of new blood vessels, and that targeting the protein can "significantly reduce" angiogenesis.

The findings have been published in the Journal of Experimental Medicine and may lead to treatments for diseases caused by excessive angiogenesis, which include AMD, said Dr Noorjahan Panjwani, who led the project.

She explained: "Our study shows that galectin-3 protein binds to glycans of specific cell-adhesion proteins to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis."

Meanwhile, another team of researchers at Tufts have found that that non-viral gene therapy can delay the onset of some forms of eye disease and offer hope to retinal degeneration sufferers.ADNFCR-1853-ID-800028486-ADNFCR

Visudyne therapy

2010-08-04T09:30:00.000-07:00

Age-related macular degeneration (AMD) is a progressive disease of the eye, meaning that it can’t be cured. The good news is that AMD can be controlled. Treatments available today can slow the vision loss associated with AMD and even restore some vision.

Wet and dry age-related macular degeneration (AMD) differ in several important respects, including treatment options. The only way to find out which AMD treatment regimen or management plan is right for you is to talk to your ophthalmologist or retinal specialist.

Visudyne therapy treats a form of AMD called predominantly classic subfoveal CNV due to AMD.

In this form of AMD, abnormal blood vessels leak fluid and/or blood under the macula—the part of the eye responsible for central vision—causing serious vision loss. During therapy, Visudyne is injected into the patient (generally through the arm). Next, light from a low-energy laser activates Visudyne, causing it to destroy the leaky vessels. As a part of a wet AMD treatment regimen, Visudyne therapy may help slow its progression.

Ask your ophthalmologist or retinal specialist if Visudyne therapy may be right for you.

Other treatment options
Anti-VEGF (anti-vascular endothelial growth factor) treatments block the formation of new abnormal blood vessels

Medicine from Moss to produce human protien

2010-07-27T08:40:00.000-07:00

Diabetics use human insulin produced in bacteria in order to treat their metabolic disorder. Many other genetically engineered proteins are also on the advance. They are being used for diagnosis as well as for therapy.

Whereas insulin used to be extracted from slaughterhouse waste, today it is produced genetically in bacteria. However, more complex proteins have to be synthesised in more complex organisms. This takes place mostly in bioreactors using animal cell lines. Biotechnologist Prof. Ralf Reski from Freiburg, Germany, has developed the moss Physcomitrella patens into a safe and inexpensive alternative supplier of medicine.

His group has now, under Dr. Eva Decker, for the first time succeeded in producing a human protein in a moss bioreactor, which has been assigned the "orphan drug" status by the respective EU authorities. This means the development and approval of such medication receive particular support from the authorities. In many people the amount of this protein decreases with old age - with severe consequences. Eva Decker explains: "With the complement factor H we have produced a protein in moss that otherwise occurs only in blood and is important for the immune system. Not enough of this protein in older people is the main cause of blindness for 50 million people worldwide. This age-related macular degeneration (AMD) is a problem, particularly in industrialised countries."

Biochemists from the Freiburg Centre for Systems Biology under Dr. Andreas Schlosser were able to show with the help of high-performance mass spectrometers that the human factor H engineered into and produced by moss was a complete protein. Infection biologists headed by Prof. Peter F. Zipfel from the Hans-Knöll-Institute in Jena, Germany, were able to prove in biological assays that factor H from moss is fully functional. "Currently factor H is not available in pharmacies, so treatment for AMD with this protein is not possible. To date recombinant production of factor H was barely feasible. I am convinced that for the first time the moss bioreactor is a promising option", says Peter Zipfel.

This work was supported by the German Federal Ministry of Education and Research (BMBF), the Freiburg Initiative for Systems Biology and the Cluster of Excellence BIOSS.
Dr. Annette Büttner-Mainik, first author of the publication, was a Kekulé scholarship holder from the endowment fund of the German Chemical Industry (FCI).
The title of the original publication is: Annette Büttner-Mainik, Juliana Parsons, Hanna Jérôme, Andrea Hartmann, Stephanie Lamer, Andreas Schaaf, Andreas Schlosser, Peter F. Zipfel, Ralf Reski, Eva L. Decker (2010): Production of biologically active recombinant human Factor H in Physcomitrella. Plant Biotechnology Journal, doi: 10.1111/j.1467-7652.2010.00552.x.

"It will take a while before medication produced in moss is available in pharmacies", says Ralf Reski, member of the Innovation Think Tank of the governor of Baden-Wuerttemberg. "We are further optimising the moss bioreactor using methods from Systems Biology and Synthetic Biology. However, the implementation of clinical studies and the setting up of industrial production is long-winded and expensive; this is the task of industry and not of university research."

Stem Cell Transplants Stalled Blindness in Rats

2010-07-20T10:21:00.000-07:00

Researchers say putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.Nerve stem cell transplants may help slow the progression of macular degeneration, the most common cause of blindness in the developed world, U.S. researchers said on Monday.

They said putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.

"These cells improve the chemical environment in the back of the eye," said Ray Lund of the Casey Eye Institute at Oregon Health & Science University in Portland, whose findings were presented at the Society for Neuroscience meeting in Chicago.

Lund said the mechanism is not clear, but he suspects that when immature nerve cells are placed near the retina, they produce growth factors that protect the cells from damage by the disease.

"It's basically a chemical pump that is sitting in the right place and producing the right things," Lund said in a telephone interview.

Where normally animals with eye disease lost their vision by three months old, rats that got the transplants kept their vision for at least seven months, he said.

"There is no evidence that they (the transplanted cells) do any damage," Lund said, adding that the animals do not develop tumors, a key worry for stem cell transplants.

The findings raise hope for use of the treatment in humans with a range of diseases in which the retina become damaged, including age-related macular degeneration or AMD, which affects nearly 30 million people worldwide, including 15 million Americans.

People with AMD lose central vision when delicate light-sensing cells of the macula, a region at the center of the retina, become damaged.

In the rats, the researchers transplanted immature nerve cells into the space near the retina. Lund said the same could be done in people with retinal disease.

Dr. Stephen Huhn, head of the Central Nervous System research program at StemCells Inc, said the cells are adult neural stem cells. He said they are multipotent, meaning they can morph into different types of nerve cells.

The company has already tested the treatment in a study of six patients with Batten's disease, a fatal inherited disorder of the nervous system.

"Having a cell that has already entered clinical testing that has been well tolerated at very high doses in the brain gives us a lot of confidence about exploring the same type of strategy in the eye," Huhn said.

Huhn said he thinks the cells may be especially well suited for use in the retina, brain and spinal cord, which are less likely to reject the cells than other parts of the body.

Ultimately, he said the hope is to develop a treatment for the dry form of macular degeneration, which affects around 90 percent of patients diagnosed with AMD. No treatments are available for this form of the disease.

Huhn said treating this form of the disease may prevent some people from developing wet AMD, in which tiny new blood vessels grow between the retina and the back of the eye.

This form of the disease can be treated with modern drugs like Lucentis, from Novartis and Roche's Genentech, and Pfizer's Macugen.

Stem cell Therapy to Benefit Blind

2010-06-30T09:32:00.000-07:00

Submitted by Jayden Roberts on Tue, 06/29/2010

Italian researchers have reported that about 12 people have regained their sight in a successful experiment conducted with some partly blind and severe eye damage suffering people. This was revealed in a study published online in the New England Journal of Medicine.

This is a remarkable success that will encourage the cell-therapy, which is done by transplanting cells from one’s own body to other parts. It has been claimed that the treatment has proved winning in 82 of 107 eyes. Also, it was partially complete in 14 others eyes. The benefits of the treatment are expected to last till 10 years after the process.

It is also noticeable that one man, who had been blind for more than five decades, have also completely restored his visual capacity. Appreciating the success, Ophthalmologist Ivan Schwab of the University of California praised and congratulated the team.

If the stem cell transplants become popular and are implemented even more, they can also prove helpful for the people who are affected by chemical burns on their corneas from heavy-duty cleansers and other chemicals. This will be a great help for people who have to suffer eyesight loss due to such mishaps.

However, the stem cell approach is not capable to treat optic nerve or macular degeneration, which is caused due to the damage in retina, as the treatment requires a few healthy tissues that can be transplanted.

Ann Arbor Pharma Firm Testing Zinc For Alzheimer's Treatment

2010-06-10T08:01:00.000-07:00

Ann Arbor-based Adeona Pharmaceuticals Inc. (AMEX: AEN) Monday announced the completion of 50 percnet enrollment in Part 2 of its clinical study, "A Prospective, Randomized, Double Blind Trial of a Novel Oral Zinc Cysteine Preparation in Alzheimer's Disease (CopperProof-2)."

The CopperProof-2 study represents the first controlled clinical study of oral zinc cysteine for the dietary management of Alzheimer's disease and mild cognitive impairment.

Part 2 of the CopperProof-2 study is designed as a 60-subject comparator study. Subjects are randomized on a 50:50 basis to receive either Zinthionein ZC or matching placebo. After 3 and 6 months on clinical trial material, serum measurements of zinc and copper are taken, and any changes in cognitive function using standard clinical tests used in Alzheimer's disease and mild cognitive impairment are recorded.

The completion of 50 percent enrollment follows Adeona's April 14 announcement of positive results from Part 1 of the CopperProof-2 study. Part 1 demonstrated a substantially lower incidence of adverse effects in Alzheimer's disease and mild cognitive impairment subjects (33 percent versus 100 percent) in favor of Zinthionein ZC (containing 150 mg of elemental zinc acetate and 100 mg of cysteine) compared to Galzin (containing either 50 mg or 100 mg of elemental zinc as zinc acetate).
Zinthionein ZC also demonstrated superior serum zinc bioavailability in Alzheimer's disease and mild cognitive impairment subjects compared to both the 50 mg and 100 mg dose levels of Galzin.

"Having pioneered the use of oral zinc therapy in dry age-related macular degeneration, which has now become the standard of care, I believe that Adeona's once-daily, high bioavailability, well-tolerated oral zinc cysteine formulation has the potential to ameliorate the sub-clinical zinc deficiency in Alzheimer's and mild cognitive impairment subjects and substantially grow current markets for oral zinc-based therapies," said David Newsome, M.D., Adeona's senior vice president for research and development.

Added Adeona CEO James S. Kuo, M.D.: "We are pleased to have reached this enrollment milestone on a timely basis and within budget. Along with the recently announced Meda collaboration for flupirtine's development and completion of 50 percent enrollment in the Trimesta multiple sclerosis clinical trial, it represents one of several major transformational changes taking place at the company in the past few months."

Observations by Adeona scientists and other scientists of sub-clinical zinc deficiency in Alzheimer's disease patients plus a body of published literature that chronic elevated copper exposure contributes to the progression of Alzheimer's disease and mild cognitive impairment prompted the present CopperProof-2 clinical study.

Alzheimer's disease can affect the entire brain but it is particularly associated with loss of tissue in the hippocampus, the area in the brain responsible for several functions including short-term memory retention and processing. The hippocampus has one of the highest concentrations of zinc in the brain. Hippocampal zinc is thought to play a role in hundreds of protective enzymes and other systems, including those that detoxify amyloid beta, an abnormally folded peptide that accumulates in aging and is a biomarker for Alzheimer's disease. When cerebrospinal fluid zinc is low, levels of the particularly toxic beta amyloid 42 are elevated.

Hippocampal zinc serves as a neurotransmitter, and also modulates a specific neuroreceptor. If the neuroexcitation goes uncontrolled, there is a derangement of brain tissue function, and possibly neuronal death. By elevating cerebrospinal fluid zinc, the receptor excitation may be better controlled, improving tissue function and thereby acute cognition and tissue survival, as may have been seen in the 1992 study. NMDA-receptor antagonists now available for Alzheimer's, including Namenda and Axura, annually sell an estimated $2.6 billion.

Zinthionein ZC is a once-daily, gastroretentive, sustained-release, oral tablet formulation of zinc and cysteine. Zinc, an essential nutrient, participates as a necessary factor in the activity of over 200 enzymes and the DNA binding capacity of over 400 nuclear regulatory elements. Zinc may also directly participate in antioxidant protection by reducing the susceptibility of sulfhydril groups to damage by oxidative free radicals. Cysteine is an amino acid that has potent anti-oxidant properties and is a necessary component of the copper-zinc-binding protein, metallothionein.

Zinthionein ZC was invented and developed by Adeona scientists to achieve the convenience of once-daily dosing, high oral bioavailability and to minimize gastrointestinal side effects associated with other commercially available, oral zinc products. All of Zinthionein ZC's constituents have GRAS (Generally Regarded as Safe) status. Adeona is developing Zinthionein ZC as a prescription medical food for the dietary management of Alzheimer's disease and mild cognitive impairment. Zinthionein ZC is protected by multiple U.S. and international pending patent applications held by Adeona.

Adeona is a pharmaceutical company developing new medicines for serious central nervous systems diseases. Adeona's primary strategy is to in-license clinical-stage drug candidates that have already demonstrated a certain level of clinical efficacy and develop them to an inflection point in valuation resulting in a significant development and marketing collaboration.

Its other drugs include Trimesta (estriol) is an investigational oral drug for the treatment of relapsing remitting multiple sclerosis, currently in clinical trials, and Effirma (flupirtine), a centrally-acting investigational oral drug for the treatment of fibromyalgia syndrome. Adeona has entered into a potential $17.5 million corporate partnership with Meda AB. As part of the agreement, Meda will assume all future development costs while Adeona is entitled to receive milestone payments and royalties.

Hyperbaric oxygen therapy and age-related macular degeneration.

2010-06-02T14:15:00.000-07:00

Weiss JN.

Retina Associates of South Florida, Margate, Florida, USA. JWEISSMD@aol.com
Abstract

Age-related macular degeneration (AMD) is a significant cause of visual loss in the United States and Western Europe. As the population ages, the prevalence rate of advanced AMD is expected to double by 2030. A one-hour session of hyperbaric oxygen therapy (HBO2) was used to treated a group of 14 patients with advanced AMD. Eight patients were treated at 1.75 ATA, and six patients were treated at 1.5 ATA for one hour. Significant improvements in visual acuity and/or visual field, with improvements in the activities of daily living were observed.

PMID: 20462142 [PubMed - in process]

Long-Term Bevacizumab Therapy in Macular Degeneration Patients Appears Safe: Presented at ARVO

2010-05-27T09:29:00.001-07:00

By Micheal Casasnovas

Most patients with neovascular age-related macular degeneration treated with bevacizumab achieved visual improvement over the course of 30 months without untoward side effects, according to a study presented here at the 2010 Annual Meeting of the Association for Research in Vision Ophthalmology (ARVO).

"This study suggests that a 30-month as-needed therapy with bevacizumab for choroidal neovascularisation in age-related macular degeneration is safe," said Renan Ferreira Oliveira, MD, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil, on May 2.

For this noncomparative, retrospective study, researchers used a consecutive case series of 20 eyes from 16 patients with choroidal neovascularisation caused by age-related macular degeneration who were treated with at least 1 intravitreal injection of bevacizumab and completed a minimum follow-up of 30 months. Patients were excluded from the analysis if they had received prior verteporfin photodynamic therapy, photocoagulation, and intravitreal or periocular injections of triamcinolone, or other antiangiogenic drugs.

Patients who received bevacizumab 1.50 mg were analysed and then examined every 30 to 90 days. Additional treatments were given if the condition worsened after originally showing a positive functional response.

Patients enrolled in this study had a mean age of 75 years (range 59-87); 62.5% were women. They received 1 to 12 injections, but the average patient was injected 5 times.

"After 30 months from the beginning of therapy, best-corrected visual acuity declined in 8 eyes [40%], improved in 7 eyes [35%], and stabilised in 5 eyes [25%]," reported Dr. Oliveira.

No significant ocular or systemic side effects occurred.

"The functional results show that 60% of patients had improved or stabilised visual acuity," said Dr. Oliveira. "However, a large proportion of patients had a vision loss in spite of close ophthalmologic control and multiple intravitreal injections of bevacizumab."

[Presentation title: Intravitreal Bevacizumab for Choroidal Neovascularization in Age-Related Macular Degeneration: 30-Month Results. Abstract A214]

Photodynamic Therapy for ARMD

2010-01-22T21:20:00.000-08:00

Photodynamic Therapy-Photodynamic therapy is also used to treat wet macular degeneration. In this procedure, a light reactive drug called Visudyne is administered through intravenous injection. The drug is activated in the eye by a non-thermal laser as it passes through the abnormal blood vessels caused by macular degeneration. The abnormal vessels are destroyed by the procedure. This procedure has largely replaced thermal laser photocoagulation. Submacular Surgery- Submacular surgery is intended to be an alternative to laser surgeries. The procedure involves physically operating on the eye to remove the blood vessels. The trials run using this method produced results that indicated that the macular degeneration treatments procedure had low success relative to laser surgery.

For more information go to www.maculardegenerationassociation.org

ForeseeHome Helps Monitor Progress of AMD Without Visiting The Clinic

2010-01-10T23:35:00.000-08:00

Globes, Israel's business newspaper, is reporting that Notal Vision out of Tel Aviv has received FDA approval for the firm's ForeseeHome age-related macular degeneration (AMD) analysis device. Designed to be used by patients at home, the device can help monitor AMD for signs of an oncoming choroidal neovascularization (CNV). It's not clear what is the functional mechanism of the device, but ForeseeHome will require a prescription and an ophthalmologist to review the results.

Published features from the product page:

•Automated, easy to use test - specifically designed for elderly people.
•Home use - familiar environment reduces anxiety and increases test frequency.
•Personalized test customized to specific user - higher sensitivity.
•Automatic analysis - immediate alert (if needed).
•Controlled environment - accurate results.
•Data export - off line, in-dept analysis capabilities.

For more information go to WWW.MACULARDEGENERATIONASSOCIATION.ORG

Laser Surgery

2010-01-04T09:43:00.000-08:00

Laser surgery for diabetic retinopathy and ‘wet’ macular degeneration(also known as macular oedema) requires a diverse system. The laser is targeted at blood vessels on the outer part of the retina.

Laser surgery is often finished in the physician’s office as an outpatient process however may also be completed in the OR in conjunction with different measures, like vitrectomy. Laser surgery is a sort of operation that employs special gentle beams rather than instruments for surgical procedures. As that occasion, many modifications have been made plus a number of different types of lasers have been produced.

Laser surgery makes use of higher intensity light pinpointed at particular attractions on the retina. Laser surgery is a therapy to aid control glaucoma(glaw- KO- muh) . You may require it if your glaucoma medications are not aiding to keep your eye pressure low sufficient. Laser surgery to correct nearsightedness can be an elective method. There is no hospital cause to have this surgical procedure. Laser surgery may open this membrane, aiding to clear vision not including an operation. This laser procedure can be named a capsulotomy.

For more information go to www.maculardegenerationassociation.org

Preventions of Eye

2009-12-14T19:10:00.000-08:00

The health of your eye muscles ultimately govern the health of your vision.Each eye has six muscles surrounding the eyeball. The eyes can move up, down, left, right, inward, and outward, always paralleling each other.Regular eye exams are crucial to your health. An eye doctor is able to examine and inform if you have any vision related, health and eye disease issues off the bat. However, a visual screening alone would not be sufficient. A complete eye exam is the only way to ensure a good bill of health.It is needless to say that our eyes are priceless. Nature has given inherent protective shields to our eyes in the form of eyebrows and eyelashes but in today's world of computers, electronic gadgets, dust and pollution we need to take extra care of this invaluable gift of God.

Myopia is an eye condition where the patient can't see clearly into the distance. It is occurs when the lens of the eye is shaped too steep, and is usually corrected with glasses, contact lenses, or LASIK eye surgery This lasik laser eye treatment operation is performed through giving the patient anesthesia drops in the eyes. During the operation the patient is awake.

Calcarea carbonicum, once per day for three days is suggested by homeopathy doctors to treat conjunctivitis for infants who suffer from other problems like seating and constipation.It is most suitable for a patient who has had several years of unchanging prescriptions. Age can preclude someone from being a candidate on this basis.
Since that time, I become a nutritionist and have learn many things about keeping eyes healthy and I plan to write an e-report so that I can pass that information on to many of you that want to avoid losing your good eye sight as you become older.One of the most common early symptoms is discomfort in the eye. A child may complain of "scratchiness", like there's something in the eye. The infection usually begins with one eye, but may spread easily to the other.

Prevention's

These kinds of reports are common. The intake of certain foods by sensitive individuals seems to cause an allergic reaction that can be revealed in the functioning of the eyes.Healthy eyesight is like a prized possession and you can prevent it from defects by diagnosing the traces of the problem in an early stage itself.

Once a year you should get your eyes checked by the ophthalmologist. Often people delay their visit to the doctor thinking that it has not yet been an year since their last visit to the doctor.In order to see sharp lines and vivid colors, to focus on reading material, and to drive safely at night, your eyes need at least 20 mg of lutein and at least one mg of zeaxanthin every day.Finding health care products and other health related websites is really easy online but remember that there's a lot of junk out there.

According to a recent report from an ongoing 5 year study by the AREDS, suggests that increased antioxidant usage has been shown to considerably slow the effects of age related vision loss and retinal disease.Eye creams are available in many forms in the market, including the usual moisturizing cream, soothing eye gels, anti-aging eye serums to brighten and tighten the fragile eye area and even eye oils to soften and replenish.

All too often though, someone will buy a special effects lens from an unreliable source to save time and money and end up suffering with a painful eye problem because of it.It was in 2002 when the first FDA-approved overnight wear corneal reshaping tool was made available to the market. The Corneal Refractive Therapy or CRT is made by Paragon Vision Sciences Inc.

Once you have established the correct measurements and the strength you can then purchase some lenses. Dark green vegetables are other good sources of lutein and zeaxanthin. Think of kale, spinach, turnip greens, collard greens, romaine lettuce, broccoli, zucchini, garden peas and brussels sprouts, corn, kiwi and honeydew.Proper eye health care can slow down the natural degenerative processes of the eyes as we grow older. In particular, macular degeneration can be reduced with the correct preventative treatments.

For more information go to www.maculardegenerationassociation.org

Protective Effects of Human iPS-Derived Retinal Pigment Epithelium Cell Transplantation in the Retinal Dystrophic Rat

2009-12-03T20:27:00.000-08:00

Transformation of somatic cells with a set of embryonic transcription factors produces cells with the pluripotent properties of embryonic stem cells (ESCs). These induced pluripotent stem (iPS) cells have the potential to differentiate into any cell type, making them a potential source from which to produce cells as a therapeutic platform for the treatment of a wide range of diseases. In many forms of human retinal disease, including age-related macular degeneration (AMD), the underlying pathogenesis resides within the support cells of the retina, the retinal pigment epithelium (RPE). As a monolayer of cells critical to photoreceptor function and survival, the RPE is an ideally accessible target for cellular therapy. Here we report the differentiation of human iPS cells into RPE. We found that differentiated iPS-RPE cells were morphologically similar to, and expressed numerous markers of developing and mature RPE cells. iPS-RPE are capable of phagocytosing photoreceptor material, in vitro and in vivo following transplantation into the Royal College of Surgeons (RCS) dystrophic rat. Our results demonstrate that iPS cells can be differentiated into functional iPS-RPE and that transplantation of these cells can facilitate the short-term maintenance of photoreceptors through phagocytosis of photoreceptor outer segments. Long-term visual function is maintained in this model of retinal disease even though the xenografted cells are eventually lost, suggesting a secondary protective host cellular response. These findings have identified an alternative source of replacement tissue for use in human retinal cellular therapies, and provide a new in vitro cellular model system in which to study RPE diseases affecting human patients.

For more information go to www.maculardegenerationassociation.org

Ohr Pharmaceutical Data Review Supports Strong Potential of EVIZON for Wet AMD

2009-11-27T11:51:00.000-08:00

As part of its drug pipeline Ohr Pharmaceutical (OTC.BB:OHRP - News) is developing a wet AMD (Macular Degeneration) therapy, based on technology acquired from Genaera Liquidating Trust. This novel therapeutic agent (EVIZON(TM)) has demonstrated the improvement or stabilization in vision in more than 100 subjects with wet AMD. Patients (wet AMD subjects) treated with at least 40 mg/m2 of EVIZON� in phase 1 and 2 studies demonstrated early signs of a biological effect: 18% had three lines or greater improvement in visual acuity 4 months after they had completed therapy and another 72% had stable vision. Throughout its clinical development, the drug was well tolerated, with no drug-related serious adverse events occurring in patients involved in this trial.

EVIZON(TM) (Squalamine for wet AMD) is a systemic anti-angiogenic therapy with a novel mechanism of action which avoids the cardiovascular and ophthalmic side effects associated with intraocular injections of anti-VEGF antibodies. As evidence of this advantage, there were no clinically significant increases in systolic or diastolic blood pressure in clinical studies of 124 wet AMD subjects receiving EVIZON� in Phase 2 clinical trials.

Wet AMD is the leading cause of legal blindness among adults age 50 or older in the Western world. Age-related macular degeneration is a progressive disease which is characterized the early stage "dry" form and the more severe "wet" form. Wet AMD is caused by the growth of abnormal blood vessels, or choroidal neovascularization, under the central part of the retina, the macula. Although the wet form of AMD accounts for only 10% to 15% of all AMD, it is responsible for 90% of severe vision loss associated with AMD. Approximately 500,000 new cases of wet AMD are diagnosed annually worldwide. In North America alone, approximately 200,000 new cases of wet AMD are diagnosed each year.

Recognizing the significant therapeutic potential of EVIZON(TM), Ohr Pharmaceutical is developing a promising novel formulation to enhance its bioavailability while maintaining its excellent safety profile.

For more information go to www.maculardegenerationassociation.org

First European patients undergo AMD treatment with NeoVista system

2009-11-16T19:23:00.000-08:00

FREMONT, Calif. — The first European patients have been treated for wet age-related macular degeneration with NeoVista's Vidion ANV Therapy System, an epimacular brachytherapy device that delivers a single dose of therapeutic radiation, the manufacturer announced in a press release.

The Vidion system is undergoing phase 3 clinical trials for U.S. Food and Drug Administration marketing approval. The device proved safe and effective in preliminary clinical trials, the release said.

Stanislao Rizzo, MD, of S. Chiara Hospital, Pisa, Italy, treated the initial group of patients with the Vidion ANV Therapy System. The release did not specify the number of patients treated or detail initial outcomes.

The Vidion system, which delivers a targeted dose of strontium-90 beta ionizing radiation to the affected area of the retina, may prove to be a viable alternative to continuous injections of anti-VEGFs, the current standard of care for wet AMD, according to the company.

The device minimizes systemic radiation exposure and exposure of adjacent tissues, the release said.

For more information go to www.maculardegenerationassociation.org

New therapy at TCD for diseases of retina

2009-11-09T09:07:00.000-08:00

Health Views

Add a commentResearchers at Trinity College Dublin have reported the development of a new drug delivery system which has the potential to treat degenerative diseases of the retina, including retinitis pigmentosa (RP), age-related macular degeneration and diabetic retinopathy.

The research was led by Dr Matthew Campbell and Professor Peter Humphries of TCD’s Smurfit Institute of Genetics and School of Genetics and Microbiology.

The new process has been used in the suppression of new retinal blood vessel growth in mice, a phenomenon called neovascularisation, which is the major sight-threatening symptom associated with age-related macular degeneration in humans.

For more information go to www.maculardegenerationassociation.org

Gene therapy transforms eyesight for 12

2009-10-27T22:08:00.000-07:00

By Thomas H. Maugh II
Los Angeles Times

Pennsylvania researchers using gene therapy have made significant improvements in vision in 12 patients with a rare inherited visual defect, a finding that suggests it may be possible to produce similar improvements in a much larger number of patients with retinitis pigmentosa and macular degeneration.

The team last year reported success with three adult patients. They have now treated an additional nine patients, including five children. The best results were achieved in the youngest patients, whose defective retinal cells have not had time to die off.

The youngest patient, 9-year-old Corey Haas, was considered legally blind before the treatment began. He was confined largely to his house and driveway when playing and had immense difficulties in navigating an obstacle course.

Today, after a single injection of a gene-therapy product in one eye, he rides his bike around his neighborhood, navigates the obstacle course quickly and has even played his first game of softball.

The results are "astounding," said Stephen Rose, at the Foundation Fighting Blindness, which supported the study. "Every individual had improvement ... and there were no safety issues at all."

The study was published online Saturday by the journal Lancet. The 12 patients suffered from Leber's congenital amaurosis, which affects about 3,000 people in the U.S. Victims are born with severely impaired vision that deteriorates until they are blind, usually in childhood or adolescence. There is no treatment.
Leber's is a good candidate for gene therapy because most of the visual apparatus is intact, particularly at birth and in childhood. All 12 of the patients suffered a defect in a gene called RPE65 that produces a vitamin A derivative crucial for detecting light.

That specific defect, which was chosen because researchers at the Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine had cloned the gene, making copies available for use.

The study, led by Dr. Katherine High, Dr. Albert Maguire and Dr. Jean Bennett of those two institutions, enrolled five people in the United States, five from Italy and two from Belgium. Five were children, and the oldest was 44.

The good copy of the RPE65 gene was inserted into a defanged version of a human adenovirus.

The engineered virus then invaded retinal cells and inserted the gene into the cells' DNA.

All the patients' vision improved. They were able to navigate obstacle courses, read eye charts and perform most tasks of daily living. The improvement has now persisted for as long as two years.

The children who were treated "are now able to walk and play just like any normally sighted child," Maguire said.

There are clear limitations to the study. The patients' vision was not corrected to normal because of the damage that had already been done to the retina, and only one eye was treated.

"The big elephant in the room is: Can you treat the other eye?" Rose said. The foundation will put more funding into the research "to make sure that if you go back and treat the other eye, it won't ablate the positive results in the first eye due to an immune reaction or something else."

Researchers also hope they will be able to translate the results to other congenital conditions using different genes. Leber's is one form of retinitis pigmentosa, which affects an estimated 100,000 Americans.

The findings might be applicable to macular degeneration, which affects an estimated 1.25 million Americans and is the major cause of visual impairment in the elderly.

For more information go to www.maculardegenerationassociation.org

A New Point-of-Care Indicator System for Dry Eye Syndrome

2009-10-22T20:55:00.000-07:00

Auxano Diagnostics, LLC, a subsidiary of Auxano Biomedical, LLC, has announced
the application of the company`s breakthrough wound care technology to the
treatment of dry eye syndrome (DES) with the Auxano point-of-care indicator
system. Dry eye syndrome (DES) is a condition that affects millions of people
worldwide. According to the Centers for Disease Control (CDC), DES can be a
serious condition, which, if left untreated, can damage ocular structures.

Brian Windsor, Ph.D., Chief Technical Officer for Auxano Biomedical, said, "We
are excited that the advances of our wound care technology can be applied to the
treatment of DES and other ophthalmic diseases. Our point-of-care indicator
system has the potential to provide earlier and more accurate guidance to
millions of DES sufferers."

Market Dynamics

Primary ophthalmic disorders associated with inflammation currently affect over
20 million people in the US. The CDC reports that the most prevalent disorders
in this category include DES, age-related macular degeneration (AMD) and
proliferative diabetic retinopathy (PDR). According to Business Insights, the
ophthalmic pharmaceutical market registered sales of $13.5 billion in 2008.

A challenge encountered in the treatment and management of ophthalmic care is
the identification between acute and chronic inflammatory diseases that lead to
visual impairment. Currently, there are no diagnostics focused on inflammatory
eye disease, and the primary way to detect inflammation is through purely
empirical methods. Misdiagnosis can lead to additional tissue damage and
potential blindness.

A solution to proper discernment between inflammatory and non-inflammatory
conditions would result in early and correct guidance towards the appropriate
therapeutic regimen, effective tracking of treatment, enhanced patient
satisfaction, and improved outcomes.

Auxano`s system is a rapid point-of-care diagnostic indicator for ophthalmic
inflammatory diseases and has the potential to provide for accurate indications
of DES within minutes.

New Ophthalmic Focus for Auxano Diagnostics

Auxano Diagnostics has developed a similar point-of-care product for wound care
that is based on the efficient and accurate detection of active enzymes in
biological samples. This product provides detection of inflammation through
targeting matrix metalloproteinases (MMPs) in wound fluids that can be obtained
by non-invasive sampling techniques. This MMP indicator is in clinical trials
through a partnership with a global technology company with the expectation of a
CE mark in December 2009, followed by FDA 510(k) approval.

Auxano`s primary focus is the adaptation, optimization and commercialization of
the existing technology for acute and chronic inflammatory diseases of the eye,
in particular, dry eye syndrome. Initial data indicates positive results for
detecting physiologically relevant MMP levels in dry eye syndrome.

For more information go to www.maculardegenerationassociation.org

OCT-guided intravitreal injection of VEGF therapy may result in less vision gain

2009-10-13T14:21:00.000-07:00

Intravitreal injection therapy with an anti-VEGF agent that is guided by optical coherence tomography may under-treat patients and result in less visual gain, according to a study.

In a population of 131 treatment-naïve eyes of 124 patients with wet age-related macular degeneration treated with Lucentis (ranibizumab, Genentech) on an as-needed basis guided by clinical examination and OCT imaging, visual improvement correlated with the number of injections delivered but not to resolution of fluid.

At baseline, the mean visual acuity for the group was 20/110, which improved at 6 months to 20/80. At last follow-up, mean visual acuity was 20/90. Also, at 6 months, 31% of eyes had gained three lines of visual acuity and 90.5% had avoided a loss of three lines.

However, eyes that received injections at an interval less than 2 months gained more vision than eyes that received injections with a greater interval. Eyes receiving injections with less than 2 months mean inter-injection interval gained 2.3 lines at 6 months compared with 0.46 lines gained among eyes with less frequent injections. Only 3.1% of patients in the more frequent injection group lost three or more lines of vision compared with 15.9% in the less frequent injection group.

For more information go to www.maculardegenerationassociation.org

Combination brachytherapy and anti-VEGF therapy demonstrates long-term safety and efficacy

2009-10-05T21:51:00.000-07:00

NEW YORK — The use of epimacular brachytherapy combined with bevacizumab appears safe for treatment of neovascular age-related macular degeneration and reduces the dosing burden of anti-VEGF therapy.

Pravin U. Dugel

After 2 years of follow-up in 34 patients treated with strontium 90 and Avastin (bevacizumab, Genentech) in a phase 2 study, 80% of patients who had cataract surgery before the study maintained vision and 30% gained significant vision. When compared with patients who had their natural lens, 65% of patients maintained vision and 20% gained significant vision.

Overall, patients received a mean 2.4 injections, including loading doses, and 76% of patients required no additional doses beyond the two required injections of bevacizumab, Pravin U. Dugel, MD, said here at the Retina Congress 2009.

For more information go to www.maculardegenerationassociation.org

Scientists cure color blindness in monkeys - humans next?

2009-09-25T18:03:00.000-07:00

By Sandra Arcaro

When English chemist John Dalton first wrote about color blindness in 1798, he must have wondered how science would improve the quality of life for people living with the condition. Today, spectacles, contact lenses and revolutionary corrective eye surgery combat the effects of a myriad of vision disorders, yet people with color blindness still live in quiet acceptance of this common genetic disorder. Now researchers have delivered promising results by successfully treating two squirrel moneys with defective color perception using a gene therapy that could also safely eradicate color blindness in humans.

Although not a particularly debilitating condition, millions of people around the world, including 3.5 million Americans, 13 million people in India and 16 million in China, are affected by color blindness. It is a congenital problem, largely experienced by men, that renders its sufferers incapable of discerning mainly red and green hues: seemingly trivial but, in reality, a necessity for everyday practicalities such as recognizing traffic lights.

The results have come to fruition after many years of collaboration between researchers from the University of Washington and the University of Florida. As explained by William W. Hauswirth, Ph.D., a professor of ophthalmic molecular genetics at the University of Florida’s College of Medicine, the gene therapy has involved adding "red sensitivity to cone cells in animals that are born with a condition that is exactly like human color blindness.”

Hauswirth’s team developed a gene-transfer technique to produce a desired protein. In this study, the monkeys Dalton and Sam, were treated with a substance called long-wavelength opsin, a colorless protein that works in the retina to produce pigments that are sensitive to red and green. Strengthening this study’s link to a human cure is the use of human DNA to avoid having to “switch to human genes as we move toward clinical treatments,” said Hauswirth.

The research team at the University of Washington, responsible for the long-term care and post-treatment assessment of Dalton and Sam’s color blindness, developed a variation of the Cambridge Color Test, the standard vision-testing technique given to school children whereby they must identify a specific pattern of colored dots among a field of dots varying in size, color and intensity. In this study, the test was modified to perfect the way the monkeys could communicate with the researchers and “tell” them which colors they were seeing.

According to Jay Neitz, professor of ophthalmology at the University of Washington, “Nothing happened for the first 20 weeks…but we knew right away when it began to work. It was as if they woke up and saw these new colors. The treated animals unquestionably responded to colors that had (previously) been invisible to them.” It has taken more than 18 months of testing the monkeys' ability to discern 16 hues, with some varying as much as 11-fold in intensity. The monkeys were able to trace color patterns on a computer touch screen and, when they chose correctly, they were rewarded with grape juice.

Even more rewarding are the wider implications of this study for other vision disorders. For example, approximately one in 30, 000 Americans has achromatopsia, an hereditary form of blindness, which causes nearly complete color blindness and extremely poor central vision. “Those patients would be targets for almost exactly the same treatment. Even in common types of blindness such as age-related macular degeneration or diabetic retinopathy, vision could potentially be rescued by targeting cone cells,” says Hauswirth. “We’ve shown that we can cure a cone disease in a primate, and that it can be done safely. That’s extremely encouraging.”

For more information go to www.maculardegenerationassociation.org

GENE REPLACEMENT SURGERY TRIAL AT UMASS MED

2009-09-18T09:36:00.000-07:00

By Aaron Nicodemus

WORCESTER
David Schwarte has been legally blind since birth. His life is not completely enveloped in darkness, as he can see through “a little patch of light at the corner of my eye.” To him, colors are washed out, shapes are blurry. He walks with a long cane.

Born with a rare genetic disorder called Leber Congenital Amaurosis, Mr. Schwarte, of West Lafayette, Ind., had few options for treatment until recently.

Through a clinical trial being conducted at the University of Massachusetts Medical School, 12 people with LCA are undergoing surgery to have a malfunctioning gene in their eye replaced with a normal gene. It is the only clinical trial of its kind in New England, one of only a handful being conducted nationwide. While the procedure is not approved by the U.S. Food and Drug Administration, the first phase of trials established that the procedure is safe. The trial is sponsored by Applied Genetic Technologies Corp. of Gainesville, Fla.

It is hoped that the trial will lead to a treatment for the estimated 20,000 to 40,000 people worldwide who have LCA.

Mr. Schwarte has been coming to Worcester regularly since July, when he had the surgery. So far, he has seen a slight improvement in his peripheral vision, and that sight is slowly moving toward the center of his eye.

“I'm still in the healing stage,” he said recently.

Dr. Shalesh Kaushal, who joined the medical school in January as its chair of ophthalmology, described the vision of people with LCA as seeing shapes and shadows, as having most colors washed out. People with LCA typically lose their vision in the first months of their lives.

“A cloudy day for most people would be like sitting in a darkened movie theater for people with LCA,” he said. “And it's a progressive disease, meaning they will continue to lose their sight over time.”

He said that gene therapy, once it has been sufficiently tested, may one day be available to address any number of gene-related disorders and diseases.

“It's a type of transforming medicine that is made possible by a confluence of a set of events,” Dr. Kaushal said. “There is any number of applications possible.”

The reason researchers have focused on curing a rare disease such as LCA, he explained, is not because it is the most common but because it is the most treatable. LCA is caused by a mutation within a single gene. Because the gene can be isolated in the eye, it can be manipulated. The exact same type of disease can be found in mice and dogs, giving scientists nonhuman test subjects.

The final piece was the development of a human virus that does not cause a disease that can be injected — with the corrected gene inside — behind the retina. The virus causes a mild immune response in most patients, he said.

Interestingly, said Dr. Kaushal, the retina's lack of an immune response works in its favor.

“When a foreign substance is introduced into human tissues and cells, it triggers the body's immune system,” he said. “Stimulation of the body's immune system can inhibit the effectiveness of gene therapy treatments and, in some cases can have adverse effects on the body and other healthy tissues. However, the retina lacks an immune mechanism, which makes treating eye diseases with gene therapy possible.”

Once the virus with the normal gene is delivered behind the patient's retina, the patient's body activates the gene. The gene then begins producing the protein necessary for the rods and cones inside the eye to recognize light. With the malfunctioning gene, LCA patients do not produce enough of this protein, and therefore their eyes do not respond to light.

Dr. Kaushal joined the medical school in January, coming from the University of Florida where he was assistant professor of ophthalmology. He is one of the first researchers in the United States to use gene therapy to treat LCA. At Florida, he and Dr. Terence R. Flotte, now dean of the University of Massachusetts Medical School, had collaborated on earlier clinical trials for this disorder.

Dr. Kaushal is a member of the Gene Therapy Center, part of the Advanced Therapeutics Cluster at the medical school. Research at the center is being applied to diseases such as cystic fibrosis; a genetic lung and liver disorder called alpha-1 antitrypsin deficiency; inherited metabolic disorders such as lysosomal storage disease; a progressive nerve disease called Canavan disease; also eye disorders such as retinal and macular degeneration.

During initial clinical trials at the University of Florida, Dr. Kaushal said all of the LCA patients saw improvement in their vision. One patient was able to read the digital clock in her parents' minivan for the first time.

“I remember one patient taking me aside and saying to me, ‘Doctor, I never knew the sky was so blue,' ” he said. “That was confirmation to me that we're on the right path.”

For more information go to www.maculardegenerationassociation.org

New therapies slows vision loss

2009-09-09T09:50:00.000-07:00

When Albert Budacz was young, he prided himself on having good eyesight; he never wore glasses. But as he eased into his late 40s, he couldn't see as well.

"I noticed a change in my vision," he explained. "Primarily in church when I would open a Bible, or something like that, I had to position myself under a light to see it."

Ophthalmologist Dr. Sharon Solomon examined Albert Budacz and found age-related macular degeneration.

Concerned that he was beginning to lose his sight, Budacz went to his ophthalmologist, Dr. Sharon Solomon with the Wilmer Eye Institute at Johns Hopkins. He was found to have the beginnings macular degeneration, an eye condition that occurs when the central portion of the retina, called the macula, begins to deteriorate.

Until recently, people with age-related macular degeneration, the leading cause of severe vision loss in Americans older than 60, had few treatment options. But now, thanks to new research and advancing technology, there are more vision-saving choices.

Early signs of macular degeneration-related vision loss include shadowy areas or fuzzy distortion in a person's central vision.

"A patient told me recently that he noticed when he was driving that the streetlights were slanted; the poles themselves were slanted," Solomon said. "That's a classic sign of the beginning of this disease."

Although obesity, smoking, high blood pressure and certain drugs can cause it, age is the primary risk factor.

"As people approach their 50s and later, they may have little yellow deposits that develop underneath the retina, and that's called drusen," Solomon explained. "Those deposits are the hallmark of what we call early age-related macular degeneration."

There are two forms of age-related macular degeneration, or AMD: the dry form, known as non-neovascular, and the wet form, called neovascular. The dry form, which Budacz has, is more common. According to the National Eye Institute, about 85 to 90 percent of patients with advanced macular degeneration have the dry form.

Dry macular degeneration is caused when drusen begin to accumulate in and around the macula. Drusen, those yellowish deposits, are debris from deteriorating tissue. With dry AMD, there is usually a gradual loss of central vision. Over a period of years, dry AMD can progress to a gradual deterioration of retinal cells, which can result in severe vision loss or lead to the wet version of AMD.

As of now, there is no FDA-approved treatment for dry macular degeneration, although a few drugs and devices are in clinical trials. However, studies have shown that supplements and a healthy diet can slow the progression of dry macular degeneration. A recent National Eye Institute study found that certain nutrients such as beta carotene (vitamin A) and vitamins C and E may reduce the risk of progression of early-stage AMD by 25 percent.

Solomon says these antioxidants have a positive effect. "They're known as 'preservision,' " she said, noting that they are commonly given to certain patient groups to slow their progression to advanced macular degeneration.

Other research has shown that B6, B12 and folic acid may help prevent age-related macular degeneration. In a study of more than 5,000 women, researchers noted those who took a combination of B6 and B12 vitamins along with a folic acid supplement had a 34 percent lower risk of developing AMD then those taking a placebo.

Although the studies showed strong results, the American Academy of Ophthalmology cautions patients to talk to their eye doctors about which supplements are best for their condition before they start popping vitamins.

In the wet version of macular degeneration, abnormal blood vessels grow beneath the retina and leak blood and fluid. This leakage causes permanent damage to light-sensitive retinal cells, which die off and create blind spots in central vision.

Doctors say it's the body's misguided way of attempting to supply the retina with more nutrients and oxygen. Instead, the attempt creates scarring, leading to severe central vision loss.

Up until recently, there's been very little doctors could do for the wet form of macular degeneration. But over the past decade, there have been a few treatments developed to slow its progression. Cold lasers are now used to freeze the abnormal blood vessels responsible for destroying the macula; they have a 60 percent success rate.

And within the past three years, researchers pinpointed a protein in the eye, called vascular endothelial growth factor, that stimulates the development of blood vessels. Injectable drugs that inhibit VEGF are now FDA-approved and available; without VEGF, there is little to encourage the growth of blood vessels in the retina.

"They actually have a 90 percent chance of stabilizing vision and a 30 to 40 percent chance of improving vision," Solomon said. "This is the first therapy that we've had that can actually [reverse] vision loss."

Most ophthalmologists prefer an ounce of prevention to a pound of cure. They promote yearly eye exams as the easiest way to keep macular degeneration in check -- and warn against waiting for a crisis to schedule a checkup.

"We typically pick up a patient when, all of a sudden, they've had an acute, abrupt loss of vision or change in the quality of their vision," Solomon said. "And sometimes it's too late."

Albert Budacz was lucky. He caught his macular degeneration in time. He's stopped smoking and takes antioxidants to slow the progression of the disease.

And although he may not have the eyesight he had as a young man, he can still see pretty well with or without glasses. And to him, that's all that matters.

For more information go to: www.maculardegenerationassociation.org

ANV therapy system receives CE mark approval

2009-09-02T18:59:00.000-07:00

Fremont, CA—NeoVista Inc. received approval from BSI Product Services to apply the CE mark to its anti-neovascular (ANV) therapy system (Vidion) to treat wet age-related macular degeneration (AMD), the company announced.

The epimacular brachytherapy device is said to be the first of its kind to receive commercial approval, according to a statement issued by the company, and it has significant implications for neovascular AMD treatment. The CE mark provides NeoVista with the ability to sell the device in all European Union (EU) countries.

“This is a momentous occasion for NeoVista as we look forward to bringing our technology to the EU with this first essential step towards commercialization,” said John N. Hendrick, president and chief executive officer, NeoVista.

“With this approval, we will begin working with our distributor network to make available our technology to the multitude of European patients currently suffering from wet AMD who are seeking an effective therapeutic option that can potentially offer a better quality of life to the patient and decrease the current burden of treatment,” Hendrick added.

The ANV therapy system delivers targeted beta radiation to leaking blood vessels, which affect central vision, without causing damage to the surrounding tissues, according to the company. This targeted epimacular brachytherapy has shown promising clinical results in preliminary clinical trials, the company said.

Learning To See With Macular Degeneration

2009-08-28T12:41:00.000-07:00

Thirteen-million Americans have AMD, age related macular degeneration, the leading cause of irreversible blindness and vision impairment in people over 50. Now, researchers started studying a new kind of therapy for AMD.

It can't reverse the damage, and it's helping patients get the most out of the vision they have left.

Macular degeneration made Russell Delong's world go black.

"To start with, I was totally blind. I couldn't see nothin'," Delong said.

Delong had surgery, but his vision was still blurry.

"Everything looked like a real heavy fog, real heavy. I couldn't see that tractor at all, I could just tell there's something there," Delong said.

After years of treatment, Delong thought he was out of options. Until, a recent study found the brain reorganizes itself to compensate for vision loss. That's the key to a new therapy that teaches patients a whole new way of seeing.

A computer maps areas of the retina damaged by macular degeneration and those that are intact. Then it trains the patient to shift his vision, using the good retinal cells to see.

"So, it's really a series of biofeedback training to get the patient to move in that positive way that we feel is going to be the most sensitive and give him or her the best vision," said Susan Primo, OD, MPH, director at Vision and Optical Service at Emory Eye Center in Atlanta, Ga.

Now with special glasses, Delong can read a magazine. Back on the farm, he can see things that used to be a blur.

"If I look at it and it's black, I turn my head a little and I see around the scar tissue, there's a tractor. I can do everything out here, everything," Delong said.

At 74, Delong still has busy days ahead, and he wants to see every second.

Researchers are currently testing the computer therapy at Emory University. Smoking, obesity and race play a role in your risk of developing macular degeneration. Whites are much more likely to lose vision from the disease than other races.

Doctors at Emory Eye Center in Atlanta, Ga., are working on a unique form of treatment for AMD that takes advantage of the brain's ability to reorganize itself to make up for vision loss. The therapy involves training AMD patients to focus on using the good cells that remain.

"We are encouraging them or influencing them to be able to use those parts of the retina to be able to better utilize the residual vision," Primo said.

In the treatment, doctors first use a computer to map out the areas of the eye that are damaged. The machine then locates the areas that are still sensitive based on factors like thickness of the retina.

The computer then uses biofeedback - in this case a series of beeps that gets faster and louder as the patient moves closer to using the healthiest portion of the eye - to train the patient to move their eye into the position that gives them the best possible vision.

New Therapy Helping AMD Patients

2009-08-04T12:53:00.000-07:00

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Content courtesy of Ivanhoe. For more information, click here.

Thirteen-million Americans have AMD -- age related macular degeneration, the leading cause of irreversible blindness and vision impairment in people over 50. Now, researchers are studying a new kind of therapy for the condition. It can’t reverse the damage, but it’s helping patients get the most out of the vision they have left.

For Russell DeLong, this would have been impossible four years ago. Macular degeneration made his world go black.

“To start with, I was totally blind," DeLong told Ivanhoe. "I couldn’t see nothin'.”

He had surgery but his world remained a blur.

“Everything looked like a real heavy fog, real heavy," DeLong said. "I couldn’t see that tractor at all. I could just tell there’s something there."

After years of treatment, he thought he was out of options. A recent study found the brain reorganizes itself to compensate for vision loss. That’s the key to a new therapy that teaches patients a whole new way of seeing.

A computer maps areas of the retina damaged by macular degeneration and those that are intact. Then it trains the patient to shift his vision, using the good retinal cells to see.

“It’s really a series of biofeedback training to get the patient to move in that positive way that we feel is going to be the most sensitive and give him or her the best possible vision," Susan Primo, O.D., Director of Vision and Optical Services at Emory Eye Center in Atlanta, Ga., told Ivanhoe.

Now with special glasses, DeLong can read a magazine. Back on the farm, he can see things that used to be a blur.

“If I look at it and it’s black, I turn my head a little and I see around the scar tissue that there’s a tractor," he said. "I can do everything out here. Everything.”

At 74, DeLong still has busy days ahead … and wants to see every second.

"I’m gonna keep going," he said.

Researchers are currently testing the computer therapy at Emory University. Smoking, obesity and race play a role in your risk of developing macular degeneration. Whites are much more likely to lose vision from the disease than other races.

for more information contact www.maculardegenertionassociation.org

Tips To Improve Your Vision – Get Rid Of Your Glasses!

2009-07-12T19:19:00.000-07:00

Eyesight improvement is achievable. You can learn to see without glasses and be relieved permanently of the pain and distress so frequently associated with defective sight. But you cannot Improve your vision by magic.

CENTRAL FIXATION

The retina is a sensitive film on which the picture falls. But there is one point on the retina where the vision is perfect; that is the Macula Lutae, a point only one-sixteenth of an inch in diameter in the very center of the retina. When we focus at this point we have what is known as central fixation and our vision is perfect.

If you have lost the capacity of central fixation you are seeing with Eccentric fixation which often causes headaches, fatigue, pain or discomfort of some kind, such as twitching of the eyelids or the eyeballs. This twitching, by the way, can be stopped by pressing the sides of the base of the nose as high as the inner canthus with the forefingers of both hands, avoiding any pressure on the eyeballs.
Continue the pressure for several minutes, with the eyes closed, and you will obtain relief.

One way of checking on whether you are seeing by central or eccentric fixation is to look at a word on this page. Do you see it most sharply where you are looking or do you see it better when you look a little away from it? When you look at the top of a printed letter do you see the bottom of the letter more clearly than the top? If so, you have lost central fixation.

If you are to see, you must bring your mind to bear on what you see. Because the eye can focus sharply and is at its maximum power only on a very small area at a time, an attempt to see a larger area results in a blurring of physical vision and a lack of mental focus. Teach yourself to look at what you see, to watch one tiny area at a time. For when the central fixation is perfect, the eye sees perfectly.

THINK ABOUT WHAT YOU SEE

For significant eye sight improvement, give the object you are looking at your mental as well as your visual attention. The more clearly it registers on your mind, the more clearly it will register on the eye.

Test this out for yourself. In the room where you are sitting there are probably a dozen objects which you no longer “see” because you are so accustomed to their presence that you are no longer aware of them. Look at each one in turn, not staring, but with quick, easy glances, thinking about what you are regarding. That doorknob-could you have described it before? Now you know its approximate size, contour, the material of which it is made, its relative position on the door, because your mind and not alone your eyes observed it.

Even such a familiar phenomenon as a moving picture gives us what we believe we see rather than what we actually see. A series of still pictures provides us with an illusion of movement.

SEE A SMALL AREA AT A TIME

Instead of staring, trying to take in a whole picture at one time and thus defeating the object of central fixation, look at one small part of the picture, shift your gaze to another small part, and another, blinking naturally all the time. The smaller the area, the more clearly you will see it.

People who have acquired bad seeing habits always try to increase their area of vision by staring, which defeats its own purpose. Staring not only causes muscular tension but a lowering of vision. You can test this for yourself by staring fixedly at an object or a word on this page. After a few moments of this effort the letters lose their sharp clarity and become blurred.

Eyesight improvement can be achieved with consistent time, effort and proper eye health care!

Regular eye exams are ‘best check’for eye disease

2009-06-06T15:37:00.000-07:00

By Sally Rummel

Chances are that sometime in your life, you will experience some of the symptoms of several common diseases of the eye. Thanks to huge advancements in technology, remarkable improvement can be experienced for most patients with cataracts, glaucoma and macular degeneration.

“So much more can be done today to treat eye disease,” said Doran Kasper, O.D., whose optometry practice has been located in Fenton for almost four decades.

Cataracts

A cataract is a clouding of the eye’s natural lens, which lies behind the iris and the pupil. The lens works much like a camera lens, focusing light onto the retina at the back of the eye. The lens also adjusts the eye’s focus, providing clear vision, both up close and far away.

*
The lens is mostly made of water and protein. The protein is arranged in a precise way that keeps the lens clear and lets light pass through it.

As people age, some of the protein may clump together and start to cloud a small area of the lens. This is a cataract, and over time, it may grow larger and cloud more of the lens, making it harder to see.

How do I know if I have cataracts?

A cataract starts out small, and at first has little effect on one’s vision. Vision may be slightly blurred, like looking through a cloudy piece of glass.

“Around the age of 50, the lens inside peoples’ eyes become cloudy enough that I can see it with my slit-lamp microscope which I use with my eye examination,” said Dr. Juan Alvarado from the Fenton Vision Center. “Eye doctors generally don’t diagnose ‘clinical’ cataracts until the cloudiness becomes vision impairing.”

A cataract may make light from the sun or a lamp seem too bright or glaring. Night drivers may notice that the oncoming headlights cause more glare than before. Colors may not appear as bright as they once did.

If you think you have a cataract, see an eye doctor for an exam to find out for sure.

When cataract surgery becomes the best option, doctors at the Michigan Eye Institute say that there are fewer than half a dozen vision practices in the state of Michigan that offer their level of experience in cataract surgery.

“We don’t use shots, needles or stitches during this 18-minute surgery,” said Dr. Bernard Tekiele. “Patients actually leave our center after surgery without an eye patch. They can expect a quick recovery with minimal limitations.

Glaucoma

Glaucoma is a category of eye disorders associated with a dangerous build-up of internal eye pressure, which can damage the eye’s optic nerve that transmits visual information to the brain.

If left untreated, patients will notice decreased peripheral vision and it can lead to blindness. In fact, glaucoma creates at least some vision loss in more than half of the approximately 2.5 million Americans who have the disease. It is the second leading cause of blindness.

Glaucoma typically causes no pain and no symptoms, often progressing without detection until the optic nerve has already been irreversibly damaged, with varying degrees of permanent vision loss.

There is no cure, but proper treatment can dramatically slow or temporarily halt its progress. Glaucoma can be treated with either medication or surgery — both aimed at lowering intraocular pressure (IOP), or pressure within the eye.

In the U.S., medications are usually the first line of glaucoma treatment. If this fails, then glaucoma surgery is the next treatment considered.

Macular Degeneration

Macular Degeneration (MD) is the most common cause of irreversible loss of central vision for senior citizens, according to the Fenton Vision Center.

The macula is located in the center of the retina — the micro-thin membrane that lines the back inside of the eye. The retina has millions of light-sensitive nerve cells that capture images focused on the retina, according to Alvarado. These captured images are transmitted to the brain by the optic nerve.

Any damage to the macula results in some loss of central vision.

There are two forms of MD:

The dry form affects about 90 percent of patients diagnosed with MD. It’s usually a gradual process that develops over the years and may affect only one eye. A person may notice more difficulty seeing with one eye than the other, a distortion of straight lines or small dark spots in the field of vision.

The wet form is less common, but has more devastating vision loss. It occurs when tiny blood vessels in the micro-thin layer of tissue beneath the retina begin to degenerate, causing tiny leaks. This can cause swelling and breaks or lesions in the retina, damaging the retina’s light-sensitive nerve cells.

“There is no cure for macular degeneration, but there are ways to help cure or delay its progression,” said doctors at the Michigan Eye Institute. Patients who have the disease or a relative with the disease are encouraged to eat a variety of green leafy vegetables, take a multi-vitamin containing lutein, and fish oil or flaxseed supplements for omega-3 fatty acids.

According to Fenton Vision Center, lasers have been used to treat the wet form of MD, but the best results come from finding the cause, and treat that to slow its progression. “We offer dialation to everyone regardless of age for all diseases,” said Alvarado. “A thorough annual eye exam is the best protection for your vision.”

Foundation Fighting Blindness’ National Neurovision Research Institute Heralds Collaboration for Gene Therapy Advancements

2009-05-10T10:01:00.001-07:00

Foundation Fighting Blindness’ National Neurovision Research Institute Heralds Collaboration for Gene Therapy Advancements

OWINGS MILLS, Md.--(BUSINESS WIRE)--The National Neurovision Research Institute (NNRI), the Foundation Fighting Blindness’ clinical trial support organization, announced today that one of its key partners, biopharmaceutical company Oxford BioMedica, has established a collaboration with sanofi-aventis, a major international pharmaceutical company, to develop and commercialize gene therapy treatments for vision-robbing retinal degenerative diseases that affect tens of millions of people around the world.

The collaboration will significantly bolster the development of the following gene therapy products: StarGen™ for the treatment of Stargardt disease, a form of early-onset macular degeneration; UshStat™ for the treatment of Usher syndrome, the leading cause of deaf-blindness; RetinoStat® for the treatment of age-related macular degeneration, the leading cause vision loss in people 55 and older in developed countries; and EncorStat™ for corneal graft rejection.

The development of treatments for these and other retinal degenerative diseases is a key goal of the National Neurovision Research Institute and is the basis for its partnership with Oxford BioMedica. In 2006, Paul and Diane Manning, with the National Neurovision Research Institute, established a partnership with Oxford BioMedica to advance gene therapies for these and other related retinal degenerative diseases.

“The investment from sanofi-aventis is a wonderful boost for the development of Oxford BioMedica’s gene therapy products and will greatly enhance our ability to move these emerging treatments into and through the clinical trial process,” says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. “This collaboration affirms the great potential for gene therapy to treat and cure a number of retinal degenerative diseases including Stargardt disease and Usher syndrome that, as rare diseases, often do not receive the attention or investment necessary to bring about promising treatments.”

“An important goal of the Foundation, through NNRI, is to attract investment from large pharmaceutical companies for the development and production of treatments for inherited retinal disease,” says Morton Goldberg, M.D., chairman of the board of NNRI. “The NNRI-Oxford partnership is an excellent model of how NNRI collaborations can accelerate the translation of laboratory-based research into clinical trials, ultimately getting successful treatments for rare diseases like inherited retinal degenerations to the market and out to the people who need them.”

Based on the agreement, Oxford BioMedica will receive approximately €43 million ($56 million) from sanofi-aventis over a three-year period. Oxford BioMedica is eligible to receive additional fees if development efforts are successful.

The treatments will utilize Oxford BioMedica’s LentiVector® gene delivery technology to deliver healthy vision-saving genes to the retina.

About Foundation Fighting Blindness

The Foundation Fighting Blindness is the largest source of non-governmental funding for retinal degenerative disease research in the world. The urgent mission of the Foundation Fighting Blindness is to drive the research that will provide preventions, treatments and cures for people affected by retinitis pigmentosa, macular degeneration, Usher syndrome, and the entire spectrum of retinal degenerative diseases. The Foundation has invested over $140 million to provide seed money for scientific research of diseases of the retina, which cause blindness. Further information is available at www.FightBlindness.org.

About National Neurovision Research Institute (NNRI)

NNRI is a recently-established non-profit support organization of the Foundation Fighting Blindness (FFB), the leading non-government funding source for inherited orphan retinal degeneration research. The mission of NNRI is to accelerate the translation of laboratory based research into clinical trials for treatments and cures of retinal degenerative diseases. It is a medical research institute that obtains support from government agencies, corporations and private foundations. It may also receive royalties or licensing fees from the drug discovery processes and commercialization of new therapies. Further information is available at www.nnri.info.

Tufts Medical Center Researchers Create a New Predictive Model for Age-related Macular Degeneration (AMD)

2009-05-03T02:09:00.001-07:00

Tufts Medical Center Researchers Create a New Predictive Model for Age-related Macular Degeneration (AMD)

BOSTON, April 23 /PRNewswire-USNewswire/ -- Researchers at Tufts Medical Center have created a formula for predicting how likely it is that individuals with certain genetic profiles and lifestyle behaviors will develop advanced Age-related Macular Degeneration (AMD), a potentially blinding condition that currently affects an estimated two million older Americans and is increasing dramatically as the population ages.

The study, led by Johanna M. Seddon, MD, ScM, Professor of Ophthalmology at Tufts University School of Medicine and Director of the Ophthalmic Epidemiology and Genetics Service at Tufts Medical Center, evaluated six genotypes that either increase or decrease risk for AMD. In addition to age, sex, and education, she also incorporated smoking status and higher body mass index (BMI) which increase risk of AMD, and supplementation with a high-dose formulation of antioxidants and zinc which delays progression of the disease. Using their new algorithm, Dr. Seddon and her colleagues determined that several genotypes plus the lifestyle factors can predict progression to the advanced forms of AMD with a certainty as high as 83%. The paper, "Prediction model for prevalence and incidence of advanced age-related macular degeneration based on genetic, demographic, and environmental variables" was published in the May issue of the journal Investigative Ophthalmology & Visual Science.

Their research also shows that although AMD has a strong genetic component, healthy behaviors can modify your genetic susceptibility. For example, among individuals with one genotype, the homozygous C3 risk genotype, the likelihood of progression to the advanced form of AMD increased from about three-fold for nonsmokers to nearly 10-fold for smokers.

"Our algorithm could help with the selection of study participants for treatment trials and could one day enable doctors to choose the most efficacious treatment for individual patients," Dr. Seddon said. "It also gives any older person concerned about AMD, or any patient with early stages or a family history of AMD, even more incentive to avoid risk factors such as smoking and excessive weight."

The study included 1,446 individuals from the Age-Related Eye Disease Study who had 6.3 years of follow-up, of which 279 progressed to the advanced stages of AMD.

About Tufts Medical Center

Tufts Medical Center is a not-for-profit, 439-bed academic medical center that is home to both a full-service hospital for adults and Floating Hospital for Children.

Othera's Eye Drop to Cure ARMD Seems Promising But Too Early to Tell

2009-04-26T03:54:00.000-07:00

Othera's Eye Drop to Cure ARMD Seems Promising But Too Early to Tell

April 16, 2009

Implications

An eye drop that stabilizes the most common form of AMD is encouraging. The ability for an eye drop to be effective is curious. Historically it has been difficult to get any medication effectively delivered to the retina via topical medications. The development of geographic atrophy is very, very slow and it is surprising that a positive trend can be noted in such a short time.
Analysis

Macular degeneration is on the rise. It is estimated that the prevalence of the disease will double in the next 40 years. Macular degeneration is often broken down into "wet" and "dry." The exudative, or wet form, involves choroidal neovascularization and is treated with anti-VEGF treatments such as Avastin, Macugen or Lucentis.

The dry form is the more common form affecting about 90% of all those afflicted with macular degeneration. The most severe of these is geographic atrophy (GA). It is a slowly progressive disease causing damage and loss of the vital underlying RPE cells. It usually takes years for patients to notice a change to their vision.

The news release describes a treatment that may be potentially helpful to most patients that are afflicted with macular degeneration. A simple eye drop to treat this disease is very intriguing. Presently, most treatments for wet macular degeneration involve direct intraocular injection of a substance as topical therapy has traditionally yielded poor drug levels reaching the retinal surface.

Clinically, it has been my experience that the disease progresses very slowly and to notice a change, for better or worse, in such a short time of two years is surprising.

Randall V. Wong, M.D.

Vigorous Exercise May Help Prevent Vision Loss

2009-04-19T05:03:00.000-07:00

Vigorous exercise may help prevent vision loss, according to a pair of studies from the U.S. Department of Energy's Lawrence Berkeley National Laboratory. The studies tracked approximately 31,000 runners for more than seven years, and found that running reduced the risk of both cataracts and age-related macular degeneration.

The research, which is among the first to suggest that vigorous exercise may help prevent vision loss, offers hope for people seeking to fend off the onset of eye disease.
"In addition to obtaining regular eye exams, people can take a more active role in preserving their vision," says Paul Williams, an epidemiologist in Berkeley Lab's Life Sciences Division who conducted the research. "The studies suggest that people can perhaps lessen their risk for cataracts and macular degeneration by taking part in a fitness regimen that includes vigorous exercise."

A cataract, which is a cloudy opacity of the eye lens, is the leading cause of blindness. More than one-half of people in the U.S. over the age of 65 suffer from some form of cataracts. Macular degeneration, which is damage to the retina, is the leading cause of irreversible vision loss in older white Americans, affecting 28 percent of people aged 75 and older.

Macular degeneration gradually destroys sharp, central vision. Macular degeneration affects the macula, the part of the eye that allows you to see fine detail. The macula is located in the center of the retina, the light-sensitive tissue at the back of the eye. The retina instantly converts light, or an image, into electrical impulses. The retina then sends these impulses, or nerve signals, to the brain. Macular degeneration causes no pain.

The diseases have several known risk factors, such as sunlight exposure and diabetes in the case of cataracts, but few interventions. Now, it appears that vigorous cardiovascular exercise may be one way to derail the diseases.

To conduct the research, Williams analyzed data collected in the National Runners' Health Study, which he established in 1991 to determine the health benefits of running.

In this case, he followed approximately 29,000 male runners and 12,000 female runners for more than seven years. Of these people, 733 men reported being diagnosed with cataracts on a questionnaire filled out at the end of the study. Too few women reported cataracts to track.

Men who ran more than 5.7 miles per day had a 35 percent lower risk of developing cataracts than men who ran less than 1.4 miles per day. The study also analyzed men's 10-kilometer race performances, which is a good indicator of overall fitness. The fittest men boasted one-half the risk of developing cataracts compared to the least-fit men.

A second study found that running appeared to reduce the risk of macular degeneration. In the study, 152 men and women reported being diagnosed with the disease. Compared to people who ran less than 1.2 miles per day, people who averaged between 1.2 and 2.4 miles per day had a 19 percent lower risk for the disease, and people who ran more than 2.4 miles per day had between 42 percent and 54 percent lower risk of macular degeneration.

"These findings are compelling because of the large size of the study, and the fact that we are looking at something that is fairly well defined: vigorous exercise, as opposed to more moderate exercise," says Williams.

Most of the runners in the study exceeded the current public health recommendations for physical activity, which is at least 30 minutes of moderate-intensity activities such as brisk walking five days a week, or smaller doses of more vigorous exercise such as running. It is unclear whether people might also lower their risk for cataracts and age-related macular degeneration by walking.

"We know there are important health benefits to walking, including lowering heart disease risk," says Williams. "It is quite likely that the studies' results might apply to a lesser extent to smaller doses of more moderate exercise."

Williams also adds that further research is needed to explore why there is a link between vigorous exercise and a decreased risk for eye disease.

"We know some of the physiological benefits of exercise, and we know about the physiological background of these diseases, so we need to better understand where there's an overlap," says Williams.

Implantable Eye Telescope Brings Sight Back To The Blind

2009-04-11T03:34:00.000-07:00

Implantable Eye Telescope Brings Sight Back To The Blind
Written on April 10, 2009 – 10:45 am | by Drew Halley |

imt_photoFor the millions of people who suffer from age-related eye degeneration, restoring sight to the blind might sound less like reality and more like a miracle. But thanks to an incredible miniature eye implant that works to restore central vision, the future’s looking bright.

The macula is a part of the retina responsible for highly detailed central vision. It contains a high density of cone cells, which allow us to perceive fine detail and quick movement in our environment - for healthy individuals, that is. Patients suffering from age-related macular degeneration (AMD) partially or totally lose this functionality, resulting in a “blind spot” where their focal point normally rests. This can make it difficult to read, recognize faces, or even watch television… until now.

The Implantable Miniature Telescope, or IMT, is a tiny prosthetic implanted into the patient’s eye. Rather than directing light to the damaged macula, the telescope projects the image onto a broader surface of the retina that surrounds the macula. In this way, visual information is redirected to healthy rods and cones, and can be processed in the brain as central vision.

Both central and peripheral vision are important functions of the visual system. Because of this, the IMT is only implanted into one eye of patients with macular degeneration. One eye continues to process peripheral vision normally (which is better suited for low-light vision, for example), while the implanted eye restores the central vision that was previously impaired. This allows individuals to again experience the full range of visual stimuli so necessary to everyday life. And because the implant is embedded in the iris, it goes unnoticed to others.

A simulation of impaired vision caused by AMD

Macular degeneration primarily effects older adults, and is the leading cause of blindness in the elderly. Nearly 15 million people suffer from AMD in the United States alone. Approximately 10% of adults between the ages of 66 and 74 suffer from AMD, a figure that jumps to 30% between the ages of 75 and 85, according to The Eye Digest.

“In an end-stage AMD population, the indicated improvements in this study are substantial compared to risks of surgery,” said study coauthor R. Doyle Stulting, M.D., Ph.D. “For patients with this level of visual impairment, the ability to be less dependent on others and to reclaim even a few of the activities they once enjoyed could make a real difference in their lives.”

The IMT was developed by VisionCare Ophthalmic Technologies, and the implant has recently completed Phase II/III clinical trials. The tests showed that the IMT doubled the vision of 2/3 of participants’ eyes (3 lines on a visual acuity chart) after one year with the implant. Some patients experienced side effects like intraocular pressure and inflammation, though these may have been related to the surgury. On March 27, an advisory panel for the Food and Drug Administration (FDA) unanimously recommended the prosthetic for approval. Barring any unforeseen events, the IMT will soon gain FDA approval and hit the market soon thereafter.

While the IMT is certainly an amazing breakthrough, it is just one of many technologies we’ve reported on that are overcoming blindness (such as bionic eyes and gene therapy). Besides the direct clinical application of such amazing technology, eye implants beg the question of how far these kinds of advances will go. Who knows? Maybe your grandkids will sport bionic eyes capable of zooming, night vision, and infrared perception. Regardless, anatomical prosthetics like the IMT promise to improve individuals’ lives today, and lay the theoretical foundation for exciting technology to come.

Purdue Professor's Insight Leads to Better Understanding of Vision Loss

2009-04-05T06:32:00.000-07:00

Purdue Professor's Insight Leads to Better Understanding of Vision Loss

WEST LAFAYETTE, Ind., April 3 (AScribe Newswire) -- A Purdue University researcher's work could shed light on new targets for treating retinal degenerative diseases that cause blindness.

According to the National Eye Institute, blindness or low vision affects 3.3 million Americans age 40 and older, and retinal degenerative diseases, such as age-related macular degeneration and diabetic retinopathy, are some of the leading causes.

Yuk Fai Leung, an assistant professor of biological sciences, co-led a team that developed a new analysis method and identified key genes involved in retinal development. A paper detailing the work was published in the Proceedings of the National Academy of Sciences last fall.

"Once we know the genetic network that influences retinal development, we can begin to understand the changes in specific genes that lead to vision loss," Leung said. "With this information, treatments could be developed that would prevent or reverse the physical affects."

Leung also recently received a $25,000 award from Hope for Vision, a nonprofit foundation that raises money to develop treatments and cures for diseases that cause blindness.

Leung led the research with John E. Dowling of the Department of Molecular and Cellular Biology at Harvard University. The research team used the analysis method to identify genes that control cellular differentiation in the retina of zebrafish.

Zebrafish are closer to humans in eye development than mice or other animal models, Leung said.

The analysis method, called factorial microarray analysis, can examine thousands of genes at once and analyze several experimental changes at the same time. Examining several changes at once is critical for understanding how one change can lead to several others, Leung said.

"Some important changes could seem insignificant if examined in isolation," he said. "For example, both eating nutritious food and swimming for an hour are good for your health. However, if you eat right before swimming, you will probably get sick. Only by doing both at the same time is the issue identified."

Additional members of the research team and paper co-authors include Ping Ma from the Department of Statistics and Institute for Genomic Biology at the University of Illinois and Brian A. Link from the Department of Cell Biology, Neurobiology and Anatomy at the Medical College of Wisconsin.

The team compared the genetic makeup of normal fish with fish that were blind due to improper development of retinal cells. The cells begin on the same track as those in the normal fish but do not complete the final stage of development known as terminal differentiation.

Leung and his team were able to identify the genetic network that controls the terminal differentiation process and to examine the effects of different combinations of genetic changes at different stages within the developmental process.

"We still don't know a lot about eye development, so we need to gather knowledge to figure out what goes wrong in a disease situation," he said. "We know the genes involved, but don't know much about the downstream changes a mutation causes. This work sets up the framework and model that can be used to examine such cause-and-effect relationships."

Leung plans to study other developments to obtain a more complete picture of eye development.

This research was funded by the Croucher Foundation, Knights Templar Foundation, Merck Award for Genomics Research, National Eye Institute and National Science Foundation.

New Hope for Preventing Age-related MD

2009-03-30T04:29:00.000-07:00

By Shahreen Abedin
CNN Senior Medical Producer

(CNN) -- Researchers may be getting closer to an effective way of preventing age-related macular degeneration, one of the leading causes of vision loss among older Americans.
A new study found that vitamins B6, B12 and folic acid may help prevent age-related macular degeneration.

A new study found that vitamins B6, B12 and folic acid may help prevent age-related macular degeneration.

A new study finds that women who took a combination of B6 and B12 vitamins along with a folic acid supplement had lower risks of developing age-related macular degeneration. The women who got the supplements, compared with those taking a placebo, had a 34 percent lower risk of developing any form of AMD, and a 41 percent lower risk of more severe forms of AMD.

Epidemiologist and study author William G. Christen, Sc.D., of Brigham and Women's Hospital and Harvard Medical School, expects that if these findings are successfully replicated in future studies, "the combination of these vitamins might become the first prevention method of early stages of age-related macular degeneration other than avoiding cigarette smoking."

Christen also noted that although the study was conducted among women age 40 and older, there is no particular reason to believe the same results would not hold true in a similar group of men.

Christen and his colleagues examined the role of vitamins B6 and B12 and folic acid in AMD partly because previous studies have shown these vitamins are known to lower levels of homocysteine, an amino acid found in the blood that when elevated has been associated with higher risks of AMD. Visit CNNhealth.com, your connection for better living

The 5,442 women who participated in the randomized, double-blind clinical trial already had heart disease or at least three risk factors for cardiovascular disease. The majority of them did not have AMD at the start of the study, which lasted more than 7 years. Christen explains that the underlying mechanism of AMD likely involves the vascular system, and researchers widely believe that cardiovascular disease and AMD share common risk factors.
Don't Miss

* Smoking quadruples risk for vision-stealing eye disease
* National Eye Institute: Age-Related Macular Degeneration

Age-related macular degeneration is a vision disease common among people older than 60, involving the deterioration of tissues in the macula, the central part of the retina. The condition impedes the performance of critical everyday functions such as reading and driving because it affects the ability to see items that a person is looking at directly, as opposed to items even a few degrees off to either side of the direct line of vision.

"If you affect that central part of your vision, no one goes blind from it but it really interferes with your quality of life," explains Dr. Roy Rubinfeld, ophthalmologist and spokesperson for the American Academy of Ophthalmology.

There are two types of macular degeneration: wet and dry. Wet forms of AMD are caused by abnormal blood vessels growing beneath the macula, which can rupture and bleed. The dry form is generally caused by cells in the macula degenerating over time and thus losing function.

While some treatments do exist for the wet form of the disease (including laser surgery, photodynamic therapy and injections into the eye), there is currently not much in the way of treatments for the more common dry form.
Health Library

When asked if the study results mean that people at high risk for AMD should begin taking a vitamin supplement that provides vitamins B6, B12 and folic acid, retina specialist Dr. Robert Frank of the American Academy of Ophthalmology suggests probably not yet.

"If you do anything, I would take a supplement of antioxidant vitamins containing high doses of vitamins A, E, C and zinc," suggests Frank, who has no financial interest in the vitamin supplement industry. These antioxidant vitamins were found to prevent the progression of age-related macular degeneration in the 10-year Age-Related Eye Disease Study conducted by the National Eye Institute of the National Institutes of Health.

However, Frank does say that while it still remains to be seen whether people currently taking a multivitamin containing the B vitamins and folic acid will be able to prevent early AMD from developing -- answers which will probably not be found for several years, after a large-scale clinical trial is begun -- there is little risk for most people in taking a daily multivitamin.

Food For The Eyes

2009-03-21T07:33:00.000-07:00

Food for the Eyes

Last Update: 3/20 1:19 pm
Source: WXYZ Detroit

Many of us plan our meals around certain foods hoping to keep our bodies healthy, but not many of us think specifically about our eyes. We have a heads up on culinary choices that can help you see better, longer. In fact, these can be called 'food for the eyes!'

Blair Carper, (worried about his vision)
"I used to be able to see things really sharp and now I don't see things as well."

He's heard carrots are good for the eyes and he's right, but they're not the only way to protect your view of the world. A recent study shows several nutrients in supplemental form help slow the progression of serious eye diseases. Ophthalmologist Sunil Srivastava says incorporating even small amounts into your regular diet can only help. One food with benefits-eggs.

Sunil Srivastava, MD, Ophthalmologist, Emory University
"Eggs do have a lot of good vitamins, such as vitamin A. Vitamin A is important in the function of the eye, specifically the retina, so vitamin A deficiencies can actually lead to night blindness."

Then there are raspberries. The vitamin C in them helps reduce the risk of cataract formation. Almonds are up next because they contain vitamin E.

Sunil Srivastava, MD, Ophthalmologist, Emory University
"Vitamin C and vitamin E have been shown to, at elevated levels, reduce the risk of things like macular degeneration in high risk patients."

Salmon or more specifically fish oil, along with green leafy vegetables, also help prevent macular degeneration, an illness that causes blindness. Ten million Americans are already coping with the disease.

Sunil Srivastava, MD, Ophthalmologist, Emory University
"Lutein and zeaxanthin are certain types of pigments that actually are concentrated in the macula of our retina, which is the center part of our vision, and foods like broccoli and spinach have high levels of lutein and zeaxanthin."

Aslo, try yogurt because the zinc in it helps the body absorb antioxidants, which also help the eyes.

Other good sources of vitamin A are cantaloupe, sweet potatoes, and mango.

Eat Better Foods to Keep Eyes Healthy

2009-03-14T06:27:00.001-07:00

March is Save Your Vision Month, sponsored by the American Optometric Association, or AOA. This year's theme is to pay more attention to nutrition to care for your eyes.

The AOA recommends increasing nutrients for healthy eyes, especially for people coping with vision loss or other eye problems.

Cataracts and age-related macular degeneration are the two leading causes of vision loss and blindness. One out of four Americans age 40 and older suffer from some level of vision loss. Patient clinical trials by the National Institutes of Health found age-related macular degeneration to be a nutrition responsive disorder. Multivitamins typically deliver nutrients below the recommended level for eye health.

Having a daily intake of certain nutrients has been linked to healthy eyes and may reduce the risk of some chronic eye conditions. Intake can be either through foods or supplements. Consult your eye health professional or physician before making changes in your diet or supplementation.

Eat foods rich in the following nutrients to help protect your eye sight and vision.

Lutein is found in colorful produce such as green beans, spinach, broccoli, oranges and corn.

Essential fatty acids are found in tuna, salmon, whole grains, lean meats and eggs.

Vitamin C is found in papaya, oranges, green peppers, and tomatoes.

Vitamin E is found in nuts & seeds like almonds, pecans, peanut butter and sunflower seeds, also sweet potatoes.

Zinc is found in whole grains, baked beans, poultry, shellfish, milk and red meat.
Renee Veksler is a Guam Memorial Hospital health educator and community partner with the Get Healthy Guam Coalition. Contact her at 647-2351.

Top Ten Healthy Things to Do for Your Eyes

2009-03-07T10:42:00.000-08:00

Top Ten Healthy Things to Do for Your Eyes
A Guide to Protecting Your Eye Health Every Day
Jennifer Palombi

Mar 5, 2009
Controlling risk for eye disease and protecting your eyes daily is important to keep your world in focus.

How often do you have your eyes examined?

Doctors agree that people should follow a consistent regimen of annual eye exams to prevent potentially serious eye complications. But what can you do the rest of the year to insure healthy eyes? This is, after all, the only pair of eyes you’ll get so they’re worth taking care of.

With that in mind, here are the top ten healthy things that you can do for your eyes:

1. See Your Eye Doctor Annually

Medical experts urge all patients with diabetes to have dilated eye exams once per year. Pupil dilation allows your doctor to see more of the inside of your eye in order to thoroughly check for signs of disease. Yet in a study performed just a few years ago, 35 percent of people had not had a dilated exam in the previous year.

2. Get Yourself a Good Pair of Sunglasses

UV radiation is harmful to the eyes and can cause cataracts. Sunglasses with broad spectrum UVA/UVB protection can help prevent harmful radiation from entering and damaging the eyes. Check with your local optical shop for a good pair of UV protective lenses. Then wear your sunglasses year round – UV radiation on the ski slopes is just as harmful as UV radiation on your favorite stretch of beach.

3. Wear Safety Glasses When the Occasion Calls For It

Whether you’re trimming shrubs in your back yard, woodworking in your garage or finally getting around to those home improvements you’ve been considering, your eyes are at risk for serious injury from flying debris. Protective glasses with polycarbonate lenses dramatically reduce the risk of eye injury associated with many of our favorite hobbies.

4. Eat Your Veggies

Your mom was right. Studies have shown that the antioxidants found in green leafy vegetables are beneficial in reducing your risk for eye diseases such as macular degeneration.

5. Control Your Blood Sugar

Stable blood-glucose levels over prolonged periods are an important factor in reducing your chance of developing a serious condition known as diabetic retinopathy. Retinopathy occurs when the blood vessels of the retina become leaky or blocked. It occurs more often in cases of poorly controlled blood glucose and can lead to severe vision loss.

6. Watch That Blood Pressure

People who suffer from hypertension can develop hypertensive retinopathy among other eye complications. By simply controlling your blood pressure, you can dramatically reduce your chances of developing eye problems.

7. Learn About All of Your Medicines

Did you know that steroid anti-inflammatory drugs (such as prednisone) can cause cataracts? Or that some drugs can cause dry eyes and still others can increase your risk for glaucoma? Know the potential complications of your medicines and be sure to report all prescription drugs and dosages to your eye doctor at each and every eye exam.

8. Wear Your Contacts as Directed

Wearing disposable lenses too long or sleeping with contacts not designed for extended-wear can put you at risk for developing vision-threatening infections. Dispose of your lenses at the prescribed interval and don’t sleep with contact lenses unless your eye doctor expressly gives you permission to do so. Most people who wear extended-wear contacts should see their eye doctors every 6 months to evaluate the health of their corneas.

9. Know Your Family History

Some eye diseases, such as macular degeneration, glaucoma and certain forms of corneal disease have a genetic link. If you have blood relatives with these conditions, you could be at higher risk for developing them yourself. Familiarize yourself with your family’s eye health history and let your eye doctor know when any new conditions develop.

10. Educate yourself!

The eyes are more than windows to the soul—they’re your windows to the world. Be mindful each day of taking these simple steps to help keep your world in focus.

For more information on eye health or to find an eye doctor in your area, contact the American Optometric Association, the American Academy of Ophthalmology at www.aao.org, or check out Prevent Blindness America’s information page.

The copyright of the article Top Ten Healthy Things to Do for Your Eyes in Patient Health Education is owned by Jennifer Palombi. Permission to republish Top Ten Healthy Things to Do for Your Eyes in print or online must be granted by the author in writing.

Read more: "Top Ten Healthy Things to Do for Your Eyes: A Guide to Protecting Your Eye Health Every Day" - http://patient-health-education.suite101.com/article.cfm/top_ten_healthy_things_to_do_for_your_eyes#ixzz095wDmELq

Advances in the treatment of wet and dry age-related macular degeneration (AMD)

2009-02-25T11:51:00.000-08:00

21 Feb 2009

Macular degeneration in the elderly (“age-related macular degeneration”, AMD) is a major cause of blindness. Its prevalence increases to 30% in patients 75 to 85 years of age. AMD occurs in two forms: dry and wet AMD. Central geographic atrophy, the “dry” form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. While no treatment is available for this condition, vitamin supplements appear to slow the progression of dry macular degeneration and, in some patients, improve visual acuity. Neovascular or exudative AMD, the “wet” form of advanced AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated. It is only recently that new drugs have been approved for wet AMD which halt progression of the visual loss or even lead to improvement. The humanized antibody fragment ranibizumab (Lucentis) directed against vascular endothelial growth factor (VEGF) was developed by Genentech and Novartis has been approved in more than 70 countries worldwide since 2006 and posted record sales of US$ 1.76 bln in 2008.

The proven effectiveness and commercial success of the anti-VEGF treatment of wet AMD has encouraged many companies to develop new treatments of wet AMD based on the proven target VEGF as well as on other experimental approaches (anti-angiogenic, anti-proliferative, anti-inflammatory). More than 20 different approaches are in clinical development and more than 20 preclinical stage projecs are under evaluation for wet AMD. Among the projects are many biologics (antibodies, peptides, proteins, antisense, DNA, cells) facilitated by the topical (intravitreal administration). Small molecule approaches may confer the convenience of oral administration but efficacy still has to be demonstrated. Fewer projects are in clinical development for dry AMD, but the most prominent ones have reached advanced clinical testing, but definitive results are still lacking.

Protect Your Eyes with Sunglasses

2009-02-17T17:14:00.000-08:00

Protect your eyes with sunglasses that offer ultraviolet protection. The second strategy is to wear 'blue blocking' glasses.

The color that blocks blue is yellow, so blue blockers must contain a yellow tint. There are ready-made "NOIR" sunglasses that block blue and UV light with a variety of tints, including:

light yellow,

dark yellow, amber, and

plum.

NOIR glasses are available as clip-ons, and as large plastic frames that fit over your regular glasses.

Avastin is inexpensive for Macular Degeneration therapy

2009-02-12T09:08:00.000-08:00

Implications:

Ophthalmologists around the country use Avastin intravitreally for wet macular degeneration in doses far smaller than those used for systemic cancer. Although it is an "off-label" use of the drug, the cost for using Avastin is 1/6oth of Lucentis, a very similar drug, also made by Genentech, that IS FDA approved for macular degeneration. Yet, Avastin works just as well as Lucentis for far less cost. I am able to get the Avastin for $50 per dose, whereas Lucentis is $3,000 per dose. So, where Avastin is expensive for a small benefit in cancer therapy, it is quite inexpensive and highly effective in the treatment of macular dengeneration.

Analysis:

Avastin, while an expensive drug, has other uses that are currently "off-label" according to the FDA. Yet the doses are small and the cost is much less than the comparable FDA approved drug. The cost issue of Avastin is an artificial one, caused by the FDA's regulatory methods. It's efficacy in both metastatic colon cancer and macular degeneration has been well shown, and the FDA is responsible for the cost differential (see "Key Implications" above). The New York Times article does not adequately address the real reasons behind the high cost of Avastin for systemic use. The FDA regulatory process is also responsible for the high cost of any medicine that carries the FDA stamp of approval. The FDA process is flawed, not the prescribers of the drug, makers of the drug, or the recipients who get substantial benefits.

EXPERIMENTAL THERAPY MAY LEAD TO MACULAR DEGENERATION, RESEARCHERS CAUTION

2009-02-05T20:23:00.000-08:00

Johns Hopkins Medicine
Media Relations and Public Affairs
Media Contacts: Maryalice Yakutchik; 443-287-2251; myakutc1@jhmi.edu
Audrey Huang; 410-614-5105; audrey@jhmi.edu
August 27, 2008

Having discovered a genetic trigger for age-related macular degeneration, the leading cause of vision loss in people over 50, researchers report that an experimental state-of-the-art therapy for treating eye disease could adversely affect the vision of some patients with the "wrong" genetic makeup.

In the August 28 online issue of the New England Journal of Medicine, a multi-institutional team, including an interdisciplinary contingent from Johns Hopkins, reports that a mutation in toll-like receptor 3 (TLR3), a protein known to help cells fight some types of infection, is associated with protection from geographic atrophy. Geographic atrophy, also known as the "dry" form of macular degeneration, is the progressive shriveling of retinal cells in the central part of the tissue called the macula where cell loss equates to irreversible vision loss.

The new study implies that there could, in fact, be adverse consequences in some individuals who undergo a new treatment using a method called RNA interference to silence genes in the wet form of age-related macular degeneration (AMD), where growth of abnormal blood vessels causes vision loss.

RNA interference (RNAi) can be used in some cases to turn off disease-causing genes. Human trials using RNAi therapy already are under way for a host of diseases, including AMD. In theory, turning off a disease gene is a good idea, but it may not be good for everyone because everyone differs in their genetic makeup, cautions Nicholas Katsanis Ph.D., an associate professor of ophthalmology, molecular biology and genetics and member of the Institute of Genetic Medicine at the Johns Hopkins School of Medicine.

"The problem is that if you happen to be an individual who has the 'wrong' genetic code in TLR3, you might inadvertently trigger a detrimental effect in your retina," he explains. "You might cure the individual of one thing and increase their risk in something else." In this case, it's possible to cure the wet form of AMD but at the same time increase risk for the other form.

"This discovery has significant implications for diagnosing the dry form of (AMD), which is the most prevalent form, affecting more than 8 million Americans," says Kang Zhang, M.D., Ph.D., a professor of ophthalmology and human genetics and member of the Shiley Eye Center at the University of California San Diego. "It also allows us to develop new drugs to treat the dry form of AMD, for which there currently is no treatment."

In the current report, the team describes experiments on mouse and human genes showing that the activity of your TLR3 can determine whether or not you're afforded a degree of protection from geographic atrophy. TLR3 is activated in response to viral infection; it causes infected cells to die. Based on one's genetic code, some people have more active TLR3 while others, less active.

"What TLR3 does in the case of infection is sacrifice an infected cell to protect the neighborhood," Zhang explains.

Biologically well-intentioned though the sacrifice may be, it can lead to blindness.

Based on previous reports hinting to TLR3 involvement in macular degeneration, Katsanis, Zhang and colleagues first set out to determine whether that link was real.

By analyzing the DNA of patients in a case-control study, the researchers not only verified previously published reports indicating an association between TLR3 and macular degeneration, but also went on to show a specific association between one "fairly common" variant of TLR3 and geographic atrophy. They found that people with specific chemical difference in the TLR3 protein were less likely to have geographic atrophy.

To test the assumption that the chemical difference rendered TLR3 less active, the researchers next used cells from human eyes containing either a "normal" or variant version of TLR3. To activate TLR3, they infected these cells with fake RNA mimicking genetic material common to many viruses, and measured how many cells died. Fifty percent fewer cells with the variant version of TLR3 died compared to cells containing the normal version, leading the researchers to conclude that the variant version of TLR3 must be less active and therefore kills fewer cells.

Finally, to be sure that differences in TLR3 activity cause similar differences in cell death in whole eyes (and not just isolated eye cells), they teamed up with the team of Jayakrishna Ambati, M.D., a professor of physiology, ophthalmology and visual sciences at University of Kentucky and injected RNA into mice, one set of which was genetically engineered to have no TLR3. Two weeks later, researchers examined their eyes and found that those mice with TLR3 exhibited 61 percent more dead eye cells than mice without TLR3, further indicating that TLR3 activity triggers cells to die, which in turn can lead to geographic atrophy.

"You and me, we have a good 20 to 30 percent chance of getting macular degeneration," Katsanis says. "So when the time comes for us to start thinking about intervention, we might want to get genotyped first, and then decide what kind of therapeutic paradigm might be most appropriate for us."

The researchers envision a day when vaccines might protect us from the viruses that trigger the pathways that are inappropriately activated or repressed in models of macular degeneration: "If we can figure out which viruses might be acting as triggers, we might be able to find a way to combat them. This would be a far more effective therapy, in my view, than trying to design a gene therapy approach," says Zhang.

The TLR3 discovery bolsters a growing body of research that illustrates how genetic information stratifies individuals for responses to particular therapies; it is the first involving the retina.

"Clearly, the statement that we're not all the same is not exactly novel, and yet, I'm still struck by how homogenized people become when it comes to clinical trials," Katsanis says. "It baffles me, frankly."

The research was funded by the National Institutes of Health, the Foundation Fighting Blindness and the Macula Vision Research Foundation, Veterans Affairs Merit Award, the Ruth and Milton Steinbach Fund, Research to Prevent Blindness, Burroughs Wellcome Fund, Clinical Scientist Award in Translational Research, and the American Health Assistance Foundation.

Other participating researchers are from Johns Hopkins University, University of California San Diego, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China, University of Utah School of Medicine, Oregon Health & Science University, University of Kentucky, Greater Baltimore Medical Center, Keck School of Medicine of the University of Southern California, and Rockefeller University.

On the Web:

http://www.hopkinsmedicine.org/geneticmedicine/

http://content.nejm.org/

Finding macular degeneration treatments

2009-01-28T10:24:00.000-08:00

Susan Slobac asked about: Finding macular degeneration treatments.

Vision problems due to the onset of macular degeneration are quite prevalent, especially in the elderly. Macular degeneration occurs when the macula, located in the central portion of the retina in the eye, becomes weakened or damaged. The result is a loss of central vision. Central vision is used to read and drive, so it is crucial to save as much of a patient’s vision as possible as soon as possible. Although this medical condition has no cure at this time, there are some promising new macular degeneration treatments that have shown to alleviate and slow down some of the symptoms of age-related macular degeneration.

There is a range of vision loss that can occur depending on the severity and type of age-related macular degeneration a patient has. Because it affects the macula located in the center of the retina, a patient’s peripheral vision is usually not adversely affected by the condition. With the onset of the condition, a patient’s vision might still be quite good, but the situation can worsen over time. There are two different types of age-related macular degeneration that often result in the greatest loss of central vision, and they are called wet and dry. The dry form of advanced macular degeneration is caused by the reduction of the rods and cones located in the retina, while wet advanced macular degeneration occurs due to leakage of excessive blood vessels and the resulting scarring under the macula.

One thing that retinal specialists might tell their patients with macular degeneration is to take certain vitamins as part of a spectrum of macular degeneration treatment s. Patients in the initial onset stages of this condition sometimes benefit from taking vitamins C, E, zinc, lutein, zeaxanthin and eating foods that are high in beta-carotenes, such as dark green leafy vegetables, corn and peas.

Another macular degeneration treatment can be found in cholesterol reducing drugs. People in the early stages of this medical condition often develop drusen, or yellow deposits, in the macula. The development and increase in the number of drusen seems to be related to the patient’s cholesterol level, with drusen more prevalent in those with higher cholesterol. Medications, such as statins, which reduce cholesterol, and aspirin, which reduces inflammation, may have a significant impact on reducing the size and number of drusen in the macula and thus lessen the chances of someone developing age-related macular degeneration.

A couple of wet advanced macular degeneration treatments, Macugen and Lucentis, have been approved by the FDA. Macugen is useful because it helps to reduce the number of excessive blood vessels that can grow under the retina. These can become inflamed and eventually burst, causing vision problems. Lucentis also reduces the growth of too many blood vessels. Lucentis is administered as an injection under the eye, and offers a great new treatment option for some patients with these kinds of vision problems.

The future is looking brighter with these emerging new macular degeneration treatments.

Seeing Machine Helps Blind See Pictures

2009-01-24T16:07:00.000-08:00

A seeing machine developed at MIT helps people with visual impairments see pictures.

Nick Barber, IDG News Service
Friday, January 23, 2009 12:00 PM PST

Using her prototype "seeing machine," Elizabeth Goldring can take pictures and see them -- with her blind eye.

After more than 20 years of work, Goldring, a senior fellow at MIT's Center for Advanced Visual Studies and her colleagues have designed a portable device that allows people with visual impairments to watch videos, access the internet, view photographs, or just see the face of a friend.

Her work started when she lost the vision in both of her eyes and doctors at the Schepens Eye Research Institute in Boston used a scanning laser ophthalmoscope, or SLO, to determine if she had any healthy retina left. The machine, which costs over US$100,000, projected images directly onto the retina of the eye, bypassing the hemorrhages contributing to her blindness.

"Technicians projected stick figures onto my retinas and I could see some of those stick figures," she said of the experience. Goldring then asked them if they could write the word "sun," which she could also see. "I was amazed. It was the first word I'd seen for months."

After her visit, she contacted and worked with the inventor of the SLO, hoping to reduce the size and cost of the device. That research yielded a $4,000 desktop model that allowed the blind to see black-and-white images. Soon after, a desktop model was created that allowed for color images to be seen. Goldring admits that version doesn't work well, but it paved the way for the current prototype.

Once a video signal is plugged into the 5-inch square box, it is then fed to an LCD panel on the inside, according to Quinn Smithwick, a postdoctoral associate at the MIT Media who has been working with Goldring on the seeing machine. The connection to the box is for a standard RCA video jack so almost anything with a video output can be plugged in. The LCD panel inside is illuminated by a bright bank of LEDs behind it, which are collimated, or traveling in the same direction. As the light passes through the LCD screen, the image pattern is "imprinted" onto the light. A lens at the back of the box focuses the light into a single point, which then enters the pupil of the eye and passes onto the retina.

"It's not that we're taking the camera image and blowing it up so you can see something big," said Smithwick. "We're trying to bypass any bad optics you may have and then get enough light and enough contrast onto the back of your retina and then you can use what little bits of retina you may have left to view it."

Goldring thinks the seeing machine could help people with macular degeneration and proliferative retinal diseases, two of the main causes of blindness in the U.S., according to Goldring. Using the device, Goldring said she can see faces and general details of people such as the color of their hair and what they are wearing. Without it, she would only know that someone is standing close to her.

Brandon Taylor, a graduate student at the MIT Media Lab, said the next step for the seeing machine is to test it with a wider population.

"We've received positive results with Elizabeth and there have been a couple other people who have used it and its been very encouraging, but what we really want to do for this testing phase is figure out what types of eye conditions this is beneficial for ... and how much improvement this machine can achieve," said Taylor. Goldring noted that there does need to be some working retina for the machine to work.

"People aren't interested in what blind people see and we have a lot of pent-up desire to express ourselves visually and this is the first step to that," said Goldring.

She and her team already have plans under way to test the seeing machine at the Low Vision Clinic at the Joslin Diabetes Center's Beetham Eye Institute in Boston. After refining the device, they would also like to make it commercially available, though are not sure when it will be or for how much. Their prototype, not including the digital camera, cost under $500 because "everything in it is already mass-produced for other purposes," Taylor said.

"Keeping the visual sense alive is something good, even if you don't use it to cross the street," Goldring said.

Improve your peripherical circulation

2009-01-14T11:50:00.000-08:00

Simon - one of my regular clients for massage - has a problem with his peripherical circulation: his feet are always cold, no matter if it is summer or winter. So, I decided to make a research in order to give him some advice on how to reduce the symptoms and I thought to share the results with you.

FOOD

Many herbal remedies such as ginkgo biloba can help improve blood circulation but so too can much of the food we eat. Five of the most effective circulation boosting foods are as follows:

1) Pumpkin seeds: they are a good source of vitamin E which research has shown can help reduce the stickiness of blood and therefore lower the likelihood of blood clots forming.

2) Oranges: the high levels of vitamin C and bioflavonoids in oranges help the flow of blood through your body by strengthening the capillary walls.

3) Nuts: they contain niacin, or vitamin B3 as it is sometimes referred to, which essentially gives your blood a boost and therefore can prevent circulation problems.

4) Watermelon and tomatoes: they are rich in lycopene which can help prevent a buildup of plaque (a substance that can interfere with blood flow) in the arteries and therefore ensure healthy blood circulation.

5) Garlic: blood circulation is another of the many strings to garlic’s bow. It can help prevent the accumulation of plaque and in some cases actively reduce it.

6) Bilberry: it has been used for centuries, both medicinally and as a food in jams and pies. It is related to the blueberry and is native to Northern Europe. Bilberry fruit contains some chemicals that have excellent antioxidant properties. They scavenge damaging particles in the body known as free radicals, helping to prevent or reverse damage to cells. Antioxidants have been shown to help prevent a number of long-term illnesses such as heart disease, cancer, and an eye disorder called macular degeneration.

EXERCISE

Regular exercise can help to reduce the symptoms of reduced peripherical circulation.

SMOKING

Stop smoking, if you smoke.

LOWER YOUR BLOOD PRESSURE

If it is too high.

REGULAR MASSAGE

Can help increase the blood flow going into the muscles.

Roberto Bocchetti is an experienced and qualified Personal Trainer and Massage Terapist in London, UK. To contact Roberto, please call +44 7508 250 126.

Dry macular degeneration

2009-01-09T14:03:00.000-08:00

Definition

Age-related macular degeneration is a chronic eye disease marked by deterioration of tissue in the part of your eye that's responsible for central vision. The deterioration occurs in the macula (MAK-u-luh), which is in the center of the retina — the layer of tissue on the inside back wall of your eyeball.

Macular degeneration doesn't cause total blindness, but it worsens your quality of life by blurring or causing a blind spot in your central vision. Clear central vision is necessary for reading, driving, recognizing faces and doing detail work.

Macular degeneration tends to affect adults age 50 and older. Dry macular degeneration, in which tissue deterioration is not accompanied by bleeding, is the most common form of the disease.

Symptoms

Dry macular degeneration usually develops gradually and painlessly. You may notice these vision changes:

* The need for increasingly bright light when reading or doing close work
* Increasing difficulty adapting to low light levels, such as when entering a
dimly lit restaurant
* Increasing blurriness of printed words
* A decrease in the intensity or brightness of colors
* Difficulty recognizing faces
* Gradual increase in the haziness of your overall vision
* Blurred or blind spot in the center of your visual field combined with a
profound drop in the sharpness (acuity) of your central vision

Your vision may falter in one eye while the other eye remains fine for years. You may not notice any or much change because your good eye compensates for the weak one. Your vision and lifestyle begin to be dramatically affected when this condition develops in both eyes.

Hallucinations

Additionally, some people with macular degeneration may experience visual hallucinations as their vision loss becomes more severe. These hallucinations may include unusual patterns, geometric figures, animals or even faces. You might be afraid to discuss these symptoms with your doctors or friends and family for fear you'll be considered crazy. However, such hallucinations aren't a sign of mental illness. In fact, they're so common that there's a name for this phenomenon — Charles Bonnet syndrome.

When to see a doctor

See your eye doctor — particularly after age 50 — if:

* You notice changes in your central vision
* Your ability to see colors and fine detail becomes impaired

One way to monitor your eyes to determine if you may need to visit your eye doctor is to check your vision regularly using an Amsler grid. This simple test may help you detect changes in your sight that you otherwise may not notice.

Here's how to perform the test:

* Hold the grid 14 inches (about 36 centimeters) in front of you in good light.
Use your corrective glasses or reading glasses if you normally wear them.
* Cover one eye.
* Look directly at the center dot with your uncovered eye.
* While looking at this dot, determine whether all of the lines of the grid appear
straight, uninterrupted and have the same contrast.
* Repeat the above steps with your other eye.
* If any part of the grid is missing or looks wavy, blurred or dark, contact your
eye doctor immediately.

Causes

The exact cause of dry macular degeneration is unknown, but the condition develops as the eye ages. The initial site of change is not in the light-sensitive cells of the macula, but in the retinal pigment epithelium (RPE), a single layer of cells located just behind the retina close to the back wall of your eye.

Your macula is an area about two-tenths of an inch (5 millimeters) in diameter at the center of your retina. This small part of your eye is responsible for clear vision, particularly in your direct line of sight.

The macula consists of millions of densely packed light-sensitive cells called cones and rods. Cones and rods have two segments: An inner segment controls cell functions and produces proteins responsive to light, and an outer segment stores and makes use of these proteins.

As they absorb light, outer segment proteins become degraded and eventually are shed as waste. Meanwhile, the inner segments continuously provide replacements for the outer segments. One function of the cells of the RPE is to remove the outer segments that are shed.

As the eye ages, cells in the RPE begin to deteriorate (atrophy) and lose their pigment. As a consequence, the RPE becomes less efficient in removing outer segment waste. When that happens, the normally uniform reddish color of the macula (as seen with an ophthalmoscope) takes on a mottled appearance. Drusen — yellow, fat-like deposits — begin to appear under the cones and rods. As the drusen and mottled pigmentation continue to develop, your vision gradually deteriorates.

Based on this progression, dry macular degeneration is categorized in three stages:

* Early stage. Several small drusen or a few medium-sized drusen are detected on
the macula in one or both eyes. Generally, there's no vision loss in the
earliest stage.
* Intermediate stage. Many medium-sized drusen or one or more large drusen are
detected in one or both eyes. At this stage, your central vision may start to
blur and you may need extra light for reading or doing detail work.
* Advanced stage. Several large drusen, as well as extensive breakdown of light-
sensitive cells in the macula, are detected. These features cause a well-defined
spot of blurring in your central vision. The blurred area may become larger and
more opaque over time.

Macular degeneration almost always starts out as the dry form. Dry macular degeneration may initially affect only one eye but, in most cases, both eyes eventually become involved.

Risk factors

Contributing factors for development of macular degeneration include:

* Age. In the United States, macular degeneration is the leading cause of severe
vision loss in people age 60 and older.
* Family history of macular degeneration. If someone in your family had macular
degeneration, your odds of developing macular degeneration are higher. In recent
years, researchers have identified some of the genes associated with macular
degeneration. In the future, genetic screening tests may be helpful for
assessing early risk of the disease.
* Race. Macular degeneration is more common in whites than it is in other groups,
especially after age 75.
* Sex. Women are more likely than men to develop macular degeneration, and because
they tend to live longer, women are more likely to experience the effects of
severe vision loss from the disease.
* Cigarette smoking. Exposure to cigarette smoke doubles your risk of macular
degeneration. Cigarette smoking is the single most preventable cause of macular
degeneration.
* Obesity. Being severely overweight increases the chance that early or
intermediate macular degeneration will progress to the more severe form of the
disease.
* Light-colored eyes. People with light-colored eyes appear to be at greater risk
than do those with darker eyes.
* Exposure to sunlight. Although the retina is more sensitive to shorter
wavelengths of light, including ultraviolet (UV) light, only a small percentage
of ultraviolet light actually reaches the retina. Most ultraviolet light is
filtered by the transparent outer surface of your eye (cornea) and the natural
crystalline lens in your eye. Some experts believe that long-term exposure to
ultraviolet light may increase your risk of developing macular degeneration, but
this risk has not been proved and remains controversial.
* Low levels of nutrients. This includes low blood levels of minerals, such as
zinc, and of antioxidant vitamins, such as A, C and E. Antioxidants may protect
your cells from oxygen damage (oxidation), which may partially be responsible
for the effects of aging and for the development of certain diseases such as
macular degeneration.
* Cardiovascular diseases. These include high blood pressure, stroke, heart attack
and coronary artery disease with chest pain (angina).

Preparing for your appointment

To check for macular degeneration, a dilated eye exam is necessary. Make an appointment with a doctor who specializes in eye care — an optometrist or an ophthalmologist — who can evaluate your condition and perform a complete eye exam.

What you can do

Appointments can be brief. Make the best use of that limited time by preparing beforehand.

* Be aware of any pre-appointment restrictions. When you make the appointment, ask
if there's anything you need to do in advance.
* Write down any symptoms you're experiencing, including any that may seem
unrelated to your vision problem.
* Make a list of all medications, as well as any vitamins or supplements, that
you're taking.
* Ask a family member or friend to accompany you, if possible. Having your pupils
dilated for the eye exam may compromise your vision for a time afterward. You
may need someone else to drive or accompany you from your appointment.

Questions to ask your eye doctor

* What kind of macular degeneration do I have?
* What is the visual acuity in my central vision?
* How advanced is my macular degeneration?
* Will I experience further vision loss?
* Will taking a vitamin or mineral supplement help prevent further vision loss?
* What's the best way to monitor my vision for any changes?
* What low-vision aids or adaptive devices might be helpful to me?

Questions your eye doctor may ask

* When did you first notice your vision problem?
* Does the condition affect one or both eyes?
* Do you have trouble seeing things near you, at a distance or both?

Tests and diagnosis

Diagnostic tests for macular degeneration may include:

* An eye examination. One of the things your eye doctor looks for while examining
the inside of your eye is the presence of drusen and mottled pigmentation in the
macula. The eye examination includes a simple test of your central vision and
may include testing with an Amsler grid. If you have macular degeneration, when
you look at the grid some of the straight lines may seem faded, broken or
distorted. By noting where the break or distortion occurs — usually on or near
the center of the grid — your eye doctor can better determine the location and
extent of your macular damage.

Regular screening examinations can detect early signs of macular degeneration
before the disease leads to vision loss.

* Angiography. To evaluate the extent of the damage from macular degeneration,
your eye doctor may use fluorescein angiography. In this procedure, fluorescein
dye is injected into a vein in your arm and photographs are taken of the back of
the eye as the dye passes through blood vessels in your retina and choroid. Your
doctor then uses these photographs to detect changes in macular pigmentation or
to identify small macular blood vessels.

Your doctor may also suggest a similar procedure called indocyanine green
angiography. Instead of fluorescein, a dye called indocyanine green is used.
This test provides information that complements the findings obtained through
fluorescein angiography.

* Optical coherence tomography. This noninvasive imaging test helps identify and
display areas of retinal thickening or thinning. Such changes are associated
with macular degeneration. This test can also reveal the presence of abnormal
fluid in and under the retina or the RPE. It's often used to help monitor the
response of the retina to macular degeneration treatments.

Treatments and drugs

There's no treatment available to reverse dry macular degeneration. But this doesn't mean you'll eventually lose all of your sight. Dry macular degeneration usually progresses slowly, and many people with the condition are able to live relatively normal, productive lives, especially if only one eye is affected. Dry macular degeneration can, however, develop into the more rapidly progressive wet type of macular degeneration at any time.

Taking a high-dose formulation of antioxidants and zinc may reduce progression of dry macular degeneration to advanced macular degeneration. The National Eye Institute-sponsored Age-Related Eye Disease Study (AREDS) showed that a daily supplement of 500 milligrams (mg) of vitamin C, 400 international units (IU) of vitamin E, 15 mg of beta carotene (often as vitamin A — up to 25,000 IU), 80 mg of zinc (as zinc oxide) and 2 mg of copper (as cupric oxide) reduced the risk of progressing to moderate or severe vision loss by up to 25 percent.
Lifestyle and home remedies

Macular degeneration doesn't affect your side (peripheral) vision and usually doesn't cause total blindness. But it can rob you of your central vision — which is important for driving, reading and recognizing people's faces. A low-vision center may be able to assess your visual capabilities and suggest certain optical and household devices that can be helpful for some near-vision tasks. Ask your eye doctor if there are any low-vision centers in your area.

There are ways to cope with impaired vision. Below are a few suggestions:

* Use caution when driving. First, check with your doctor to see if driving is
still safe based on your current visual acuity. When you do drive, there are
certain situations to avoid. For example, don't drive at night, in heavy traffic
or in bad weather.
* Seek help traveling. Use public transportation or ask family members to help,
especially with night driving.
* Travel with others. Contact your local area agency on aging for a list of vans
and shuttles, volunteer driving networks or ride shares.
* Get good glasses. Optimize the vision you have with the right glasses, and keep
an extra pair in the car.
* Use magnifiers. Large-print books and magazines can help you read more easily.
* View with large type on the Internet. Look for Web sites that use large-sized
type fonts, or change the font size on your display.
* Obtain specialized appliances. Some clocks, radios, telephones and other
appliances have extra-large numbers.
* Have proper light in your home. This will help with reading and other activities.
* Remove home hazards. Eliminate throw rugs and other possible tripping hazards in
your home.
* Ask friends and family members for help. Tell them about your vision problems so
that they can help you perform certain tasks and help you recognize people.
* Don't become socially isolated. A common frustration of people with macular
degeneration is the inability to recognize other people and greet them by name.
If this happens to you, try asking people you know to say hi and tell you their
names when you meet them on the street or in other situations so that you can
greet them back.
* Take advantage of online networks. The Internet is a good source for support
groups and resources for people with macular degeneration.

Alternative medicine

Some people have turned to complementary or alternative therapies, such as bilberry, ginkgo and shark cartilage, in the belief that they can help prevent the progression of macular degeneration.

However, there's no conclusive evidence that any of these products are effective for macular degeneration, and some may interact with other medications you're taking. Check with your doctor before taking any dietary or herbal supplement.
Prevention

The following measures may help you avoid macular degeneration:

* Eat foods containing antioxidants. Foods with antioxidants are those rich in
vitamins A, C and E. People who eat diets rich in vegetables, particularly leafy
green vegetables, may have a lower risk of macular degeneration. The National
Eye Institute is currently sponsoring a clinical trial to assess the efficacy of
three specific antioxidants — lutein, zeaxanthin and omega-3 fatty acids — in
lowering the risk of macular degeneration. Lutein and zeaxanthin are found in
high concentrations in egg yolks, corn, and spinach and other green leafy
vegetables. Omega-3 fatty acids are found in fish as well as other foods such as
almonds.
* Take antioxidant and zinc supplements. For people with moderate to advanced
macular degeneration, findings from the National Eye Institute-sponsored
Age-Related Eye Disease Study (AREDS) indicate that taking high doses of zinc,
beta carotene, and vitamins C and E is effective in reducing the risk of further
vision loss. However, beta carotene has been linked to increased risk of lung
cancer in smokers. Too much vitamin E can be toxic. Ask your doctor about these
supplements before trying anything on your own.
* Eat fish. A diet rich in the omega-3 fatty acids found in fish can result in a
reduced risk of macular degeneration.
* Stop smoking. Smokers are more likely to develop macular degeneration than are
nonsmokers. Ask your doctor for help to stop smoking.
* Manage your other diseases. For example, if you have cardiovascular disease or
high blood pressure, take your medication and follow your doctor's instructions
for controlling the condition.
* Get regular eye exams. Early detection of macular degeneration increases your
chances of preventing serious vision loss. If you're older than 40, get an exam
every two to four years, and older than 65, every year or two. If you have a
family history of macular degeneration, have your eyes examined more frequently.
* Screen your vision regularly. If you've received a diagnosis of early-stage
macular degeneration, your doctor may suggest that you regularly monitor your
vision at home with an Amsler grid. Doing so may help you to detect subtle
changes in your vision at the earliest possible time and seek help promptly.

If you have some vision loss because of macular degeneration, your eye doctor can prescribe optical devices called low-vision aids that will help you see better for close-up work. Or your doctor may refer you to a low-vision specialist. In addition, a wide variety of support services and rehabilitation programs are available that may help you adjust your lifestyle.

By Mayo Clinic Staff
Aug. 26, 2008

Common Treatments for Macular Degeneration

2009-01-03T11:08:00.000-08:00

In this section, you will find information on:

* Angiogenesis Inhibitors
* Laser Photocoagulation
* Photodynamic Therapy
* Vitamin and Mineral Supplements

Angiogenesis Inhibitors

Angiogenesis Inhibitors are used to treat the wet form of macular degeneration. The two most commonly used are Lucentis® (ranibizumab injection) and Macugen® (pegaptanib sodium injection).

Lucentis®

Generic name: ranibizumab injection

Year approved by the FDA: 2006

Effective for: Wet age-related macular degeneration (AMD)

How it works: Vision loss in wet AMD is caused by the growth of abnormal leaky blood vessels that eventually damage the macula (area of the eye responsible for central vision). Lucentis is an antibody fragment that binds to and inhibits the activity of human vascular endothelial growth factor (VEGF), a protein believed to play a critical role in the formation of these new blood vessels. Lucentis is injected into the vitreous portion of the eye (the clear jelly-like substance that fills the eye from the lens back to the retina). In AMD, VEGF is continually produced, so routine administration of Lucentis over a period of time is required.

Most common side effects: The most commonly reported adverse events included hemorrhage of the conjunctiva (the membrane that covers the white part of the eye), floaters, eye pain, increased eye pressure and inflammation of the eye. Serious adverse events such as endophthalmitis (severe inflammation of the interior of the eye), retinal detachment, retinal tear, increased eye pressure and traumatic cataract are rare.

Status: Avastin®, a drug manufactured by the same company that makes Lucentis (Genentech, Inc.), has been used by physicians as an “off-label” treatment for AMD, but is actually an FDA-approved cancer therapy. Both drugs are similarly administered. However, Avastin costs much less, and many physicians believe these drugs are equally effective. The National Eye Institute of the National Institutes of Health is planning to conduct clinical trials in 2008 (Comparison of Treatments Trials or CATT) to study the relative efficacy and safety of Avastin and Lucentis.

Macugen®

Generic name: pegaptanib sodium injection

Year approved by the FDA: 2004

Effective for: Wet age-related macular degeneration (AMD)

How it works: Vision loss in wet AMD is caused by the growth of abnormal leaky blood vessels that eventually damage the macula (area of the eye responsible for central vision). Macugen blocks vascular endothelial growth factor (VEGF), a protein that promotes this blood vessel growth.

Macugen is injected into the vitreous portion of the eye (the clear jelly-like substance that fills the eye from the lens back to the retina). In AMD, VEGF is continually produced, so ongoing, routine administration of Macugen is required.

Most common side effects: Common side effects of Macugen include inflammation of the eye, blurred vision or changes in vision, cataracts, bleeding in the eye, swelling of the eye, eye discharge, irritation or discomfort of the eye and "spots" in vision.

Laser Photocoagulation

Year approved by the FDA: 1991

Effective for: Wet age-related macular degeneration (AMD)

How it works: Photocoagulation was the first treatment that was used for wet AMD. During this outpatient procedure, the eye is numbed, and a high-energy laser heats, seals and destroys abnormal leaky blood vessels. This can help prevent or slow further damage, but it results in a permanent blind spot. When successful, laser photocoagulation is a one-time treatment. However, if new blood vessels grow, surgery may have to be repeated.

Most common side effects: Some patients experience mild pain during and shortly after the procedure. This is usually relieved by taking non-prescription pain medication. Reduced vision and scarring of the retina may also occur.

Status: It is not possible to treat those with “subfoveal” AMD in which the abnormal blood vessels are located under the fovea, in the center of the macula. Almost 90% of AMD is subfoveal, so only a small percentage of patients are candidates for this procedure.

Photodynamic Therapy

Visudyne® Generic name: verteporfin

Year approved by the FDA: 2000

Effective for: Wet age-related macular degeneration (AMD)

How it works: Photodynamic therapy (PDT) using Visudyne ® (verteporfin) is widely used to treat the new growth of fragile and abnormal blood vessels or neovascularization that is characteristic of wet AMD. PDT is most effective for a subtype of AMD called predominantly classic subfoveal, in which areas of abnormal blood vessel growth and bleeding in the fovea, at the center of the macula, are well-defined. The great majority of AMD cases are subfoveal, but only 25% of these cases are the predominantly classic subtype.

During the PDT procedure, Visudyne, a light-sensitive drug, is injected into a vein in the arm. The drug enters the bloodstream and is absorbed by the abnormal blood vessels growing underneath the macula. A low-intensity, non-thermal (“cold”) laser is then directed at the retina for a little over a minute. This activates the Visudyne allowing it to destroy the abnormal vessels and inhibit the neovascularization. The cold laser does not damage the retina or other cell layers that overlie the abnormal vessels. PDT may help to stabilize vision, but it will not restore lost vision and is not likely to improve vision. Treatments are typically administered every 3 months and as many times as needed to prevent re-growth of the abnormal vessels (potentially 6-7 treatments over 2-3 years). One treatment normally takes about 20 minutes and is relatively painless.

Most common side effects: The most common side effects of PDT include headache, injection site reaction, and possibly blurred or reduced vision. Because the drug is activated by light, patients must avoid exposing their eyes or any part of their skin to sunlight or bright indoor light for up to five days after treatment.
Status: To date, the FDA has only approved Visudyne for PDT. Other light-sensitive drugs are being evaluated, and researchers are also studying the use of verteporfin in combination with other types of therapies.

Vitamin and Mineral Supplements

Year approved by the FDA: The Food and Drug Administration (FDA) regulates dietary supplements under a different set of regulations than those covering conventional foods and drugs (prescription and over-the-counter). Dietary supplement manufacturers are responsible for ensuring that a dietary supplement is safe before it is marketed; the FDA may take action against any unsafe supplement after it reaches the market. Generally, however, manufacturers do not need to register their products with FDA nor get FDA approval.

Effective for: Intermediate dry age-related macular degeneration (AMD)

How it works: Currently, there is no treatment or cure for dry macular degeneration. However, in 2001, the National Eye Institute’s (NEI’s) Age-Related Eye Disease Study (AREDS) found that taking a specific high dose formula of vitamins and mineral supplements (AREDS formula) significantly reduced the risk of progressing from intermediate macular degeneration to advanced or wet macular degeneration. The study showed no benefit for those with early stage macular degeneration.

When macular degeneration progresses to the advanced stage, toxic substances build up that may damage the retina. The vitamins and minerals of the AREDS formula act as antioxidants to help maintain healthy cells and tissues and may prevent this damage. In the study, the effective formula contained 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene, 80 milligrams of zinc as zinc oxide and two milligrams of copper as cupric oxide.

Many of the antioxidants in the AREDS formula can be found in over-the-counter vitamin and mineral supplements, but the dosages required to achieve maximum efficacy are far greater. AREDS formula supplements may be contra-indicated with medications and patients should consult a physician before taking any vitamins or minerals. Patients with intermediate macular degeneration in one or both eyes or advanced macular degeneration in one eye but not the other eye might consider taking the formula.

Most common side effects: Some participants in the AREDS clinical trials reported minor side effects. A small percentage of those given zinc treatments developed urinary tract problems that required hospitalization. Yellowing of the skin, a well-known side effect of large doses of beta-carotene, was reported slightly more often by participants taking antioxidants.

Status: NEI is currently recruiting 4,000 volunteers to participate in AREDS-2 trials. The study will focus on the effect of adding two supplements, lutein and zeaxanthin, as well as two omega-3 long chain fatty acids (DHA and EPA) to the original AREDS formula. Researchers are interested in the effect of these supplements on the progression to advanced macular degeneration and/or moderate vision loss in those at risk of progression. Participants will also be offered variations on levels of beta-carotene and zinc to the original AREDS formula. Scientists will follow up for at least five years.

Disclaimer: The information provided in this section is a public service of the American Health Assistance Foundation, and should not in any way substitute for the advice of a qualified healthcare professional and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. The American Health Assistance Foundation does not endorse any medical product or therapy.

Source: The information provided in this section of our website was obtained from the National Eye Institute of the National Institutes of Health and ClinicalTrials.gov. The American Health Assistance Foundation is grateful to Jeffrey H. Stern, M.D., Ph.D. at the Regenerative Research Foundation in Rensselaer, New York for reviewing aspects of the above content.

Last Reviewed On: 11/21/08

Baran Brothers: Going for Green Keeps Vision Golden

2008-12-27T20:50:00.000-08:00

We interact with the marvelous world around us in numerous ways. Without a doubt, our visual contact with the universe may be the most gratifying. We have as a species developed this “visual” side to our senses, causing it to dominate all others. Beyond the aspect of seeing the beauty around us, however, eyesight cripples us when it begins to fail.

Age-related macular degeneration, or ARMD, causes almost half of all cases of impaired vision or blindness in this country. This disease, which causes the macula (part of the retina that controls central vision) to gradually break down, is chronic and degenerative.

There are two types of ARMD: “dry” and “wet,” with over 90% of cases being of the form characterized by progressive deterioration of the retina (dry). Although laser treatments seem to benefit the wet version of the disease, there is very little in the way of treatment for the more common dry form. There is some good news, however, as research is beginning to suggest various nutrients and supplements may help to slow or stop the disease.

A controlled study reported in Optometry (2004;74:1-15) found that supplementation of lutein, either combined with antioxidants and other nutrients or alone, actually improved vision in people with ARMD, in both early and advanced stages.

Lutein is in the carotenoid family of molecules (most famous of these being beta carotene) and in the body actually concentrates itself in the macula portion of the retina. There it filters out the very damaging blue light component of sunlight. It is found in large amounts in kale and spinach, and in lesser amounts in other dark green leafy vegetables, egg yolk, and corn.

In the study, 90 people with ARMD were divided into three groups and were given daily treatments for 12 months. Group 1 received 10 mg of lutein daily (amount present in about two ounces of spinach); group 2 received the same amount of lutein coupled with nutrients to enhance retinal health, such as antioxidants, bilberry, quercetin, taurine, zinc, N-acetyl cysteine and others; group three was the placebo control.

For both groups receiving lutein there was an improvement in visual acuity (equivalent to an improvement of up to one line on a standard eye chart) and in contrast sensitivity. Using certain parameters, combination therapy seemed more effective than lutein alone, and using other measures lutein by itself seemed more effective. Both active groups showed an improved capacity to filter out toxic blue light, and both showed beneficial effects in both early and later stage ARMD subjects.

Because lutein is a potent antioxidant, it may possess health related benefits beyond eye health. Studies now suggest that lutein may possibly protect the circulatory system from deadly plaque build-up, rejuvenate lungs, lower the risk of arthritis of the knee, protect an aging brain, and help to reduce oxidative damage to the skin. Another closely related antioxidant, called zeaxanthin, also concentrates itself in the macula and is typically found in the same food sources as lutein. When supplementing with lutein, look for products that supply zeaxanthin along with lutein. Researchers typically recommend five to 10 mg of lutein per day for optimum eye health.
As always consult your physician or health care practitioner in all these matters that impact your health, seek corroboration of information, and most of all, educate yourself.

Andre Baran IV and his brother Bernard Baran, are co-owners of Brothers Nutrition in Edgewater. They can be reached via e-mail at edge@
brothersnutrition.com.

Eye Health 9 Simple Ways to Keep Your Eyes Healthy

2008-12-23T10:07:00.000-08:00

Do you eyes feel tired and sore by the end of the day? Modern life puts a lot of stress on our bodies and eyes are among the first things to suffer. But it doesn't have to be this way. Learn simple things you can do for your eye health and your eyes will feel and look much better in only a few days.

Have your eyes checked every 12 month

Uncorrected vision problems can progress, and wearing corrective contact lenses or glasses that are no longer right for you can cause vision problems and severe headaches.

If your contacts don't feel right in your eyes, it is probably time to visit an eye doctor, even if it hasn't been a year since your last visit.

Go for the best quality contact lenses

Not all contact lenses are equal. Some are safe for you, while others put you at risk of damaging your eyes.

See reviews of quality contact lenses. Knowing what the modern contact lens industry has to offer will help you make an educated choice, not just blindly follow what your doctor says.

In summer, always wear sunglasses

It is proven that UV rays can seriously damage your eyes, but good sunglasses can prevent this damage. When buying sunglasses, make sure that they block at least 98% of UV radiation. Contrary to popular belief, light sunglasses can block UV as well as very dark ones, even though dark glasses usually offer more protection against bright sunlight.

By the way, did you know that you need sunglasses on cloudy days as well? Clouds might provide shade, but they are no barrier for UV light. Clouds are basically water, and water is UV-transparent.

Finally, remember that you would need sunglasses even if your contact lenses offer UV protection. Even a very high quality lens can only protect the area it covers, but the entire surface of your eye needs protection.

Eat what is good for you and your eyes

The good news is that there are no foods that would be harmful for your eyes. Most foods don't affect your eyesight at all, although the right vitamins and minerals are helpful. Recent studies have shown that vitamins of the antioxidant group can prevent, or at least slow down, age-related conditions like macular degeneration and the development of cataracts. So a healthy diet won't restore eyesight that is already lost, but it can definitely slow down the process of the disease, or prevent one from starting.

Vitamins C, A and E, folic acid, selenium and zinc are definitely beneficial for the health of your eyes. The effects of the other vitamins and minerals aren't determined yet, but it seems likely that they affect your eyesight as well. Thousand-page books have been written on the topic of nutrition for eye health but, to summarize, it is known that whatever is good for your body is good for your eyes, too. So put a carrot and a bunch of grapes into your lunch box.

When you read or work on the computer make sure that the light is right

It is a common knowledge that working with poor light can cause eyestrain, but light that is too bright can do as much damage.

Keep your blinds down on sunny days and switch off half of the household lights, if possible. The best lighting for working on the computer is a soft desk light, coming from the side. Also, you can try decreasing the brightness of your monitor. The colors won't be so vivid, but your eyes will feel much better by the end of the day

Give your eyes a health break

The great invention of the 20th century - computers - is not so great from the point of view of health. Almost everybody feels discomfort in their eyes after peering at a computer screen all day long. This is because people blink about 25% less often then usual, while working at the computer, which causes eye dryness.

I won't advise you to blink more often - it is almost impossible to control natural reflexes. One thing you can do, though, is close your eyes and count to 5 before opening them, whenever your computer decides to take its sweet time doing something. Another thing is to look away from the screen and focus on some faraway object, as often as possible. If you train yourself into the habit, your eyes should feel much better at the end of your working day.

If you wear contact lenses, take proper care of them

Contact lenses don't require a lot or fuss, but you can't neglect their cleanliness. Every time you put your lenses in or take them out, rinse them. You should also take care to change the solution, when you are putting your lenses to rest for the night.

Wear your contact lenses to the recommended schedule

Daily disposable lenses should be replaced daily, two weeks replacement lenses should be replaced every two weeks, and so on. Some people try to save money by wearing their lenses for much longer than is intended. This isn't a good idea. Even though the quality of the lens itself might not decline, protein build-up will make your vision less clear. Another thing to consider is that the longer you wear your lenses, the higher is your risk of eye infections.

There are other ways to save on your contacts without risking your eye health. See suggestions on how to get discount contact lenses.

Try not to wear your contact lenses from 6 in the morning until midnight. Most lenses aren't designed to be worn for longer than 12 hours. If this doesn't suit your life style, though, try using extended wear lenses. You can wear Acuvue contacts for a week without removing them, or Focus Night and Day lenses for up to 30 days.

If you want to change the color of your eyes, choose only top quality color contact lenses

Color contact lenses are great fun. If you didn't try them yet, maybe you should. But only high quality color contacts, like Freshlook or Acuvue 2 Colors, are as safe and comfortable as they are beautiful. Many beauty salons, however, sell color contacts lenses of questionable quality, and these can do serious damage to your eyes.

If you follow these simple rules, your eyes should feel much better. They will look better too - you might notice that your eyes shine and their whites are actually white, again.

Macular Degeneration Study Links Behavior, Visual Improvement

2008-12-16T09:25:00.000-08:00

Jim Burress ATLANTA, GA (2008-12-11) Gina Lembo is an attractive and energetic 30-year old with Stargardt's Disease, a form of macular degeneration that appears in childhood.

"I see a clear picture; however, it's my peripheral. So we have a central vision loss."

It's unlikely Gina's condition will worsen. That's not the case for most macular degeneration, or "M-D", patients who develop it later in life. Their vision loss starts as a dark, central blur that expands over time.

So, like most with M-D, Gina uses her peripheral vision to compensate for her loss in central vision.

"So we don't see blank, we see a full picture, but it's going to look as though I'm looking to the left or up or down and not straight at you, when I feel I am"

Helping at her brother's pizza parlor in Norcross, Gina demonstrates how she compensates. It's a process of using peripheral vision, memorizing her surroundings and relying on her acute sense of touch as she demonstrates while cutting a lime.

"I very much use my sensory. I don't realize I do. And when people watch me they'll get very nervous that I'll slash my wrist or break something. But I have a system that works, and I've always done it that way."

Gina's brain--and her eyes--made her a perfect candidate for participation in a study by Georgia Tech and Atlanta's Emory Eye Center.

"The question we asked was, 'Does using those peripheral regions cause a change in the brain?'"

That's Eric Schumacher, a Georgia Tech psychology professor and the study's author.

He and a graduate student wanted to know how M-D patients' use of peripheral vision potentially re-wired their brains.

"It'll be different area in different patients, but it will tend to be stable within a patient they'll tend to choose one region to use as their PRL." meaning the part of the eye they use to see best.

Now this is where the science comes in. What we see straight-on largely comes from the part of our eye called the fovea. This fovea 'thing' lets us see small and vivid details, things like words on a page or the color of a traffic light.

But seeing is only partly done with the eye.

What the fovea senses is carried to the very back of the brain where the images are put together. It's an area just loaded with neurons that get all excited when we see. But in a patient with macular degeneration, those neurons don't get stimulated because the fovea doesn't send along any information.

Instead, they just sit there.

What the team found, though, is that that by identifying and stimulating parts of the eye that are strongest, those bored neurons can become re-energized.

"So that's the idea that something about the change in their behavior that they begin to use this one peripheral region drives reorganization of the primary visual cortex to begin to activate to that region."

In other words, the part of the brain the fovea stimulates in most people can become the same area M-D patients use. They won't see perfectly. But they might see better.

Dr. Susan Primo of the Emory Eye Center says the next step is to take that science to the bedside.

"...and in turn the patients will be trained to use that particular point and then to be able to use that every day in functioning, whether it is for work, school or for reading."

While science has long known the brain can reorganize itself, this study is the first to show a person's behavior can directly reorganize the brain, at least as it relates to vision.

Researchers stress the results are small steps in a long journey

Jim Burress, WABE News.

NEW YORK (Reuters Health) Nov 27 - Patients who lower their waist-to-hip ratio, particularly those who are obese, can decrease their odds of developin

2008-12-12T20:23:00.000-08:00

A new study indicates that the carotenoids lutein and zeaxanthin may help improve vision under glare conditions such as bright sunlight or the beams of car headlights.

Scientists at the Vision Science Laboratory at the University of Georgia recently studied the relationship of lutein and zeaxanthin on macular pigment (MP), glare disability, and photostress recovery.

The macula helps filter damaging light rays. When the concentration of lutein and zeaxanthin in the macula is higher, the higher density of macular pigment enables the macula to absorb the light rays more efficiently.

Researchers studied forty healthy subjects (average age of 23.9) for six months, giving assessments at baseline, 1, 2, 4, and 6 months. Subjects were given 12mg daily of lutein and zeaxanthin supplements.

After 6 months, the lutein and zeaxanthin supplementation was shown to significantly reduce the negative effects of glare for both the visual performance tasks assessed for most of the subjects.

Read other studies about lutein and zeaxanthin, including their role in preventing macular degeneration and cataracts.

Learn more about natural leutein and zeaxanthin supplements

SOURCE: “Macular pigment and visual performance under glare conditions”, Stringham and Hammond, Optom Vis Sci., 2008 Feb;85(2):82-8

Flexible Dosing of Ranibizumab Safe, Maintains Efficacy in Age-Related Macular Degeneration: Presented at AAO

2008-12-09T08:55:00.000-08:00

By Emma Hitt, PhD ATLANTA -- November 12, 2008 -- A flexible dosing schedule for ranibizumab maintains efficacy outcomes in treatment-naïve patients with neovascular age-related macular degeneration (AMD), according to research presented at the American Academy of Ophthalmology (AAO) annual meeting.

Frank G. Holz, MD, University of Bonn, Bonn, Germany reported findings from the phase 3b Study of Ranibizumab in Patients With Subfoveal Choroidal Neovascularization Secondary to Age-Related Macular Degeneration (SUSTAIN) here at an oral session on November 11.

SUSTAIN was designed to assess the safety and efficacy of ranibizumab in choroidal neovascularisation secondary to AMD, using a guided, individualised, as-needed, dosing schedule.

The study included 531 individuals who were either ranibizumab-naïve or had completed the Anti-VEGF (vascular endothelial growth factor) Antibody for the Treatment of Predominantly Classic Choroidal Neovascularization in AMD (ANCHOR) trial.

The current analysis was a preplanned interim analysis of 69 of the ranibizumab-naïve patients. Patients received 3 fixed monthly injections of either 0.3 or 0.5 mg ranibizumab in the initial phase and then returned every 4 weeks in the maintenance phase for a total study period of 12 months.

Criteria for retreatment in the maintenance phase included visual deterioration greater than 5 letters or a greater than 100-mcm increase in central retinal thickness.

Ocular adverse events occurred in 55.1% of study eyes and were mostly mild in nature, Dr. Holz explained during his presentation. Adverse events included reduced visual acuity, transiently increased intraocular pressure, retinal or conjunctival haemorrhage, and blepharitis. Serious adverse events included a retinal haemorrhage in one patient and retinal pigment epithelium detachment in another patient.

In ranibizumab-naïve patients, visual acuity was maintained over the course of 12 months using guided, individualised, as-needed dosing; there was a decrease from 9.2 letters to 6.7 letters from months 3 to 12, but this difference was not significant. Likewise, the decrease in central retinal thickness was maintained, with a decrease of 89.6 mcm at month 3 and 78.7 mcm at month 12.

The average number of injections given in the initial phase was 3.0 (range: 2 to 3) and 2.3 (range: 0 to 7) in the maintenance phase, indicating that only minimal doses are needed when using a flexible dosing schedule.

At month 3 and month 12, the change in visual acuity from baseline was within 15 letters for approximately 74% and 71% of patients, respectively, indicating that as-needed treatment maintained visual acuity.

"These results suggest that flexible dosing based on predefined treatment criteria with monthly monitoring results in fewer injections overall and can maintain efficacy outcomes," said Dr. Holz.

Funding for this study was provided by Novartis Pharmaceuticals Corporation.

[[Presentation title: Flexibly Dosed Ranibizumab in Patients With Neovascular AMD: Twelve-Month Interim Results of the SUSTAIN Trial. Abstract PA078]

Canadian Bio Med Systems, Inc. Opens $10 million funding project, for two new drugs for the treatment of eye diseases

2008-11-22T18:20:00.000-08:00

By: PR Newswire
Nov. 17, 2008 09:01 AM

NEW YORK, MONTREAL and SAN DIEGO, CA, Nov. 17 /PRNewswire-FirstCall/ - Canadian Bio Med Systems Inc., a subsidiary of ICBS Limited (OTCPK: ICBT),) announced $10 million funding project for the development of two new drugs for age related macular degeneration (AMD) , and Glaucoma, being developed in conjunction with the university of Arizona .

Canadian Bio Med Systems, Inc. (CBMS) today announces that it is developing a drug to help cure the leading cause of blindness for persons over 50 years of age, for macular degeneration of the eye. The drug is being developed in conjunction with its partner Ocular Therapeutics, Inc. of San Diego, CA. The company has opened a $10 million dollar funding project through ICBS, which is targeting Federal funding along with private equity sources.

The company is currently involved in talks with a major Canadian University to work in conjunction with the University of Arizona. The company will also be taking advantage of the Research & Development grants offered by the Quebec and Canadian governments that will refund up to 70% of the companies R&D costs.

Wet age-related macular degeneration (AMD) is one of the leading causes of severe vision loss and blindness in the adult population. In the United States, there are more than 1.6 million cases of wet AMD and approximately 200,000 new cases of wet AMD are reported each year. A majority of wet AMD patients experience dramatic vision loss within months after diagnosis. Because AMD generally affects adults over 50 years of age, it is expected that the incidence of AMD will increase as the baby-boom generation ages and life expectancy increases and it has been estimated by the National Eye Institute that by 2030, an estimated 2.8 million Americans will suffer from visual impairment as a result of AMD.

While several treatment options for wet AMD are available, each has its disadvantages such as increased risk of stroke, failure to show improvement, and cost. There is no indication that any of these drugs is effective enough that it obviates the need for additional drugs to treat this disease, leaving the opportunity for novel new compounds to enter the market. The advantage of the drug under development at CBMS lies in the unique mechanism by which it manages the cause of AMD, inhibition of migration, which is distinct from the current treatments. This drug, therefore, will not compete directly with other marketed treatments and may be used as a replacement for or in conjunction with these therapies to increase the efficacy of treatment.

Glaucoma is the second most common cause of blindness in the United States, accounting for (greater than)11% of all cases of blindness in the country. The various glaucomas are estimated to affect (greater than)2.2 million individuals in the United States who are (greater than)40 years old with primary open angle glaucoma, the most common form. Glaucoma is the leading cause of blindness among African-Americans, and African-Americans are three to five times more likely to have the disease than Caucasians.

"These new compounds being developed by our two companies can be quite important in treating this very debilitating ocular diseases" said Dr. Richard Keates, MD, Chairman of Ocular Therapeutics. "Because of the unique method of action, it has the capability of becoming a very large component in the treatment of AMD and Glaucomas"

NB. This news release includes statements that constitute forward-looking statements. Please be aware that any such forward-looking statements are not guarantees of future performance and involve significant risks and uncertainties, and that actual results may vary materially from those in the forward-looking statements as a result of any number of factors, including the risk factors contained in the Company's disclosure documents.

SOURCE Inter Canadian Business Service

My sister went to a naturopathic physician who gave her an intravenous infusion of nutrients. What's this all about?

2008-11-22T18:17:00.000-08:00

Vitamins, minerals, and other nutrients are administered intravenously for a wide range of health conditions. It is a safe, inexpensive and effective means to deliver nutrients.

Why isn't oral supplementation sufficient?
Oral supplements and medication are convenient to take, but they are only as good as one's digestive and absorptive capabilities. When there are problems with digestion and assimilation, the recipient may be getting only a fraction of the intended benefit. When this happens, intravenous nutrients can be useful in treating illnesses that do not respond to other therapies. Additionally, some illnesses are best treated with nutritional concentrations higher than one could achieve with oral administration, and intravenous infusions can deliver a concentration of a nutrient that could not be obtained with an equivalent oral dose.

What conditions are treated with intravenous infusion?
Intravenous nutrition can be helpful in treating fibromyalgia, chronic fatigue and exhaustion. It is beneficial in supporting the immune system and treating the symptoms of the common cold, flu, and other viral illnesses. Macular degeneration and glaucoma are also improved with intravenous nutritional therapy as well as Parkinson's disease and arrhythmias of the heart. It has tremendous benefits is tissue and would healing, arresting asthma and as adjunctive treatment for many cancers.

Hanna Ian, M.S., N.M.D, is a naturopathic physician. She is in private practice at
The Naturopathic Physician located in Surprise. Reach Dr. Ian at 623-792-8889 or www.thenaturopathicphysician.com.

Age Related Macular Degeneration Therapy

2008-11-22T18:12:00.000-08:00

(a) Laser Photocoagulation:
This procedure uses laser to destroy the fragile, leaky blood vessels. A high energy beam of light (argon or krypton laser) is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. Though thermal laser treatment has been shown beneficial at reducing the likelihood of developing severe visual loss, there is usually an immediate decrease in visual acuity especially in subfoveal choroidal neovascularization (CNV). A CNV membrane is described as subfoveal if any part of the lesion lies beneath the centre of the foveal avascular zone (FAZ). The concern of subfoveal lesions is due to the fact that photocoagulation of such a CNV membrane necessarily results in the destruction of the overlying retina.2 Moreover, thermal laser is effective only in a small subgroup of patients with small, well-demarcated lesions that include a component of classic CNV. Therefore, many alternatives to laser photocoagulation are evolving mainly for subfoveal CNV.

(b) Photodynamic Therapy (PDT):
In 2000, USFDA approved Visudyne™ (Verteporfin for injection) for the treatment of predominantly classic subfoveal choroidal neovascularization due to AMD, pathologic myopia or presumed ocular histoplasmosis. It was the first approved drug therapy for the treatment of wet AMD. Visudyne™ is injected systemically and activated by a non-thermal laser to destroy leaking vessels.3 This therapy utilizes low-intensity light exposure (689 nm, 50 J/cm2 dose, for 83 s in Verteporfin PDT) which causes selective destruction of CNV with preservation of the overlying neuro sensory retina. There are various photosensitizing agents available for treatment. However, currently only Verteporfin is approved for the treatment of CNV. 4 Patients who receive this therapy become temporarily photosensitive and should avoid direct sunlight for 5 days.

(c) Anti Vascular endothelial growth factor (anti-VEGF)
VEGF is a naturally occurring large lipoprotein molecule consisting of at least 6 structurally related proteins. Studies have shown elevated VEGF levels in areas of laser induce CNV in primates and clinically in AMD patients. Macugen (Pegabtanib) was approved in 2004 to treat wet AMD, and is used solely or in combination with other AMD treatments.

The drug Lucentis (Ranibizumab) was approved by FDA for treating AMD in June 2006. It is a humanized antibody fragment designed to bind and inhibit the action of VEGF and thus prevent blood vessel growth and leakage. Avastin (Bevacizumab) is a drug similar to Lucentis that is used to treat colon cancer. Ophthalmologists may prescribe Avastin off label for the treatment of AMD.

VEGF Trap is a substance that blocks the action of vascular endothelial growth factor (VEGF), and prevents the growth of new blood vessels in a tumor. It belongs to the family of drugs called angiogenesis inhibitors. Angiogenesis is the term used to describe the proliferation of blood vessel growth. Substances that stop the growth of excessive blood vessels are anti-angiogenic .Bayer Healthcare and Regeneron have initiated a Phase 3 study of the VEGF Trap -Eye in the neovascular form of wet AMD. 5

(d) Combination therapy of Triamcinolone and Verteporfin
Triamcinolone acetonide has been used to modify the process of choroidal neovascularization. Corticosteroids have a multitude of anti-inflammatory effects and also seem to have direct anti-angiogenic properties. Steroids have an inhibitory effect on angiogenesis, fibrotic activity and inflammatory reaction by reducing the migration and activation of inflammatory cells. Up-regulation of extracellular matrix protein plasminogen activator inhibitor by steroids results in direct angiostatic effect. Corticosteroids stabilize endothelial and basement membranes and also reduce vascular permeability with beneficial effects.

PDT provides immediate angio-occlusion of CNV and intravitreal triamcinolone acetonide (IVTA) , prevents inflammation and up-regulation of VEGF, decreases subsequent regrowth of CNV and finally improves VA outcome. This provides substantial reasons for using verteporfin and triamcinolone in combination. 6, 7,8

Significant improvements in best-corrected visual acuity (VA) after 1 month and their maintenance over a 3-month period were observed after verteporfin Photodynamic therapy combined with intravitreal bevacizumab. These results should be confirmed in larger and long-term prospective randomized trials. 9

Alternative Therapies:

(a) Radiation Therapy:
Radiotherapy affects the evolution of exudative macular degeneration directly by endothelial toxicity, leading to capillary closure and/or indirectly through its attenuating effects on the inflammatory response, mediated by macrophages and other inflammatory cells.10 Low-dose ionizing radiation has been shown to prevent proliferation of endothelial cells of newly formed subretinal capillaries and may induce destruction of abnormal CNV tissue.

(b) Submacular Surgery:
Surgical removal of CNV with large subfoveal hemorrhages can limit toxicity to overlying photoreceptors by prompt evacuation of blood . 11 By preserving the overlying neurosensory retina it can limit visual field defect enlargement and central vision loss.
Moreover,surgery may apply to a wide range of lesions and adjunctive procedures such as RPE transplantation. However, the risks with submacular surgery are considerable and include acceleration of cataract, development of retinal tears and retinal / choroidal detachments.

(c) Retinal translocation:
Retinal translocation and limited macular translocation are being used with rationale to move the macular area from the underlying CNV to a healthier RPE region. The Choroidal neovascular membrane can then be treated with laser photocoagulaton, while sparing the foveal center. 12 However, there is risk of development of intractable proliferative vitreoretinopathy, total retinal detachment, and unpredictable long-term visual prognosis.

(d) Transpupillary thermotherapy (TTT):
A slit lamp delivery system is used to project a beam of diode laser on the lesion thereby causing heat transmission to RPE and choroid. Studies by Reichel et al 13 showed benefit for patients with occult CNV in terms of improvement of visual acuity and decreased exudation.

Prevention:
There is evidence that dietary supplements can help prevent the onset and progression of age-related macular degeneration. Lutein and zeaxanthin is found in leafy green vegetables, corn, egg yolk, squash, broccoli and peas. These carotenoids are proposed to reduce the risk of AMD by absorbing the blue light that could damage the macula, by preventing free radicals from damaging eye cells and by strengthening eye cell membrane. 14

Undergoing Research
Research is in progress to transiently enhance vascular permeability in PDT to selectively release an anti-angiogenic or anti-inflammatory factor to prevent recurrence of neovasculature in case of AMD or to release chemotherapeutic agents in the case of PDT of a malignant tumour. 15
A study was done to evaluate the safety, efficacy & durability of systemic Bevacizumab therapy for neovascular ARMD. The results were good for a small group of patients however the risks associated with systemic anti-VEGF therapy versus the safety of intra vitreal therapy deters the involvement of a large number of patients. 16

Micro and nano particulates have been used primarily on a pre-clinical basis as new drug delivery devices in experimental models of neovascular AMD 17 .The development of polymeric micelles with smart functions such as environment-sensitivity and specific tissue-targetability may enhance the activity of potent bioactive compounds, facilitating their clinical applications. Also, polymeric micelles response to external stimuli, such as light, might exert the activity of the loaded compounds in a site-directed manner, ensuring the effectiveness and safety of the nanocarrier-mediated targeting therapy. Thus, polymeric micelle-based nanocarriers will continue to hold promise for the delivery of drugs and genes . 18

All types of nucleic acids have been developed for the treatment of infectious and cell proliferative diseases affecting mostly the posterior segment of the eye. The eye is therefore a good target for this type of molecules mainly because it is a confined compartment and their delivery is close to the target site. However, to improve the efficiency of such molecules, the use of controlled and/or targeted delivery systems is needed since they allow protection against degradation, increase intracellular penetration and permit long-term delivery avoiding repeated administrations. 19

Conclusion:
Early detection of AMD can stop the progress of the disease. Patients need to be educated about the condition and consistent follow up is required. Drug delivery to the posterior segment of the eye still remains a challenge. Rapid pre corneal elimination, poor corneal absorption, rapid anterior chamber elimination and large diffusional path lengths combine to prevent topically administered drugs from reaching the posterior segment of the eye.

Lot of research is being undertaken and many Pharmacophores are being investigated. A fundamental understanding of the patho physiology of AMD integrated with a mechanistic understanding of drug delivery to the posterior segment is requisite for the design of drugs and drug delivery systems for macular degeneration.

References:
1. Verma L, Das T, Binder S. Heriot W.J., New approaches in the management of choroidal neovascular membrane in age-related macular degeneration, Current Ophthalmology, (48) (4) (2000) 263-78.
2. Beatty et al, Photocoagulation of subfoveal choroid neovascular membrane in age related macular degeneration, British Journal of Ophthalmology (83) (1999) 1103-1104.
3.Orest O., Patrick H., Drug delivery strategies to treat age related macular degeneration, Advanced drug delivery reviews (57) (14) (2005) 1991-1993.
4. Kulkarni A. D., Kuppermann B. D., Wet age related macular degeneration, Advanced drug delivery reviews (57) (14) (2005) 1994-2009.
5. http://www.fiercebiotech.com/press-releases/press-release-bayer-healthcare-regeneron-initiate-phase-3-vegf-trap-
6. Kumar A., Visual acuity and contrast sensitivity outcomes in Indian eyes undergoing photodynamic therapy with intravitreal injection of triamcinolone acetonide in age-related macular degeneration, Indian journal of ophthalmology (55) ( 3)(2007) .
7.Gillies M. C. ,Sompson J. M. ,Luo W, Penfold P., Hunyor A. B.,Chua W., A randomized clinical trail of a single dose of intravitreal Triamcinolone Acetonide for neovascular age-related macular degeneration: One-year results. Arch Ophthalmol (121) (2003) 667-673.
8. Jonas J. B.,Kreissing I.,Hugger P., Sauder G , S. Panda-Jonas, Degenring R., Intravitreal triamcinolone acetonide for exudative age-related macular degeneration, British Journal of Ophthalmology (87) (2003) 462-468.
9.Lazic R., Gabric N., Verteporfin therapy and intravitreal bevacizumab combined and alone in choroidal neovascularization due to age-related macular degeneration, Ophthalmology (114) ( 6) (2007) 1179-1185.
10. Munshi A. , Age related macular degeneration: A study of patients managed with radiotherapy, Journal of cancer research and therapeutics (3) (1) (2007) 12-16
11. Lewis H , Intraoperative fibrinolysis of submacular haemorrhage with tissue plasminogen activator and surgical drainage, American.Journal of Ophthalmology (118) (1994) 559-568.
12. Potter M., Improvement in macular function after translocation surgery in a patient with age-related macular degeneration, American Journal of Ophthalmology (129) ( 4) (2000) 547-549
13. Reichel E.,Berrocal A. M ,Desai V., Duker J.S. ,Pulfiafito C. A, Transpupillary thermotherapy of occult subfoveal choroidal neovascularization in patients with age related macular degeneration, Ophthalmology (106) (1999) 1908-1914.
14. http:// www.nutraingredients .com Europe 16/08/2006.
15. Debefve E., Combination therapy using aspirin-enhanced photodynamic selective drug delivery, Vascular Pharmacology (46) (3) (2007) 171-180.
16. Rosenfeld J. P, Systemic bevacizumab (Avastin) Therapy for neovascular age-related macular degeneration twenty-four-week results of an uncontrolled open-label clinical study, Ophthalmology (11 ) (113) (2006) 2002-2011.
17. Moshfeghi A.A ,Peyman G. A., Micro and nano particulates, Advanced Drug Delivery Reviews (57) (14) (2005) 2047-2052.
18. Nobuhiro N; Current state, achievements, and future prospects of polymeric micelles as nanocarriers for drug and gene delivery, Pharmacology and Therapeutics (112) (3) (2006) 630-648.
19. Fattal E. , Ocular delivery of nucleic acids: antisense oligonucleotides, aptamers and siRNA, Advanced Drug Delivery Reviews (58) (11) (2006) 1203-1223.

Angiogenesis Inhibitors

2008-11-21T08:35:00.001-08:00

Lucentis^® (Generic name: ranibizumab injection)

Year Approved by the FDA: 2006

Effective for: Wet macular degeneration

How it works: Lucentis^®is an antibody fragment that binds to and inhibits the biologic activity of human Vascular Endothelial Growth Factor A (VEGF-A), a protein that is believed to play a critical role in the formation of the new abnormal and leaky blood vessels, characteristic of wet macular degeneration. The drug is injected into the vitreous portion of the eye (the clear jelly-like substance that fills the eye from the lens back to the retina). Due to the fact that the production of VEGF-A is ongoing, routine administration of this drug is required.

According to data collected during clinical trials, nearly 95 percent of the participants who received a monthly injection maintained their vision at 12 months following the beginning of treatment compared to approximately 60 percent of patients who received the control treatment. Approximately one-third of patients in these trials had improved vision at 12 months.

Most common side effects: The most commonly reported adverse events included hemorrhage of the conjunctiva (the membrane that covers the white part of the eye), floaters, eye pain, increased eye pressure, and inflammation of the eye. Serious adverse events such as endophthalmitis (severe inflammation of the interior of the eye), retinal detachment, retinal tear, increased eye pressure and traumatic cataract were rare and often related to the injection procedure. There is also a small increase in the risk of stroke. Clinical trial data indicated that approximately .3 percent of patients suffered a stroke when given a .3 milligram dose of Lucentis^®compared to 1.2 percent of patients who received a .5 milligram dose. In addition, patients who have previously suffered a stroke may be at greater risk of having another stroke.

Potentia Pharmaceuticals' Drug Candidate for Age-Related Macular Degeneration Shows Positive Safety Profile in Phase I Clinical Trial

2008-11-21T08:08:00.000-08:00

AMD Patients Treated with POT-4 Demonstrate No Adverse Toxic Effects

Last update: 10:21 a.m. EST Nov. 10, 2008

ATLANTA, Nov 10, 2008 /PRNewswire via COMTEX/ -- Potentia Pharmaceuticals, a privately held biotechnology company developing medicines for the treatment of age-related macular degeneration (AMD), presented Phase I data last week during the Retina Subspecialty Day at the American Academy of Ophthalmology (AAO) Annual Meeting in Atlanta, GA. The data was from the ASaP (Assessment of Safety of Intravitreal POT-4 Therapy for Patients with Neovascular Age-Related Macular Degeneration) clinical trial for the company's leading drug candidate, POT-4, which is being developed for the treatment of AMD.

The ASaP trial is a first-in-man, multi-center, single escalating dose study. The interim results of this trial revealed no drug-related toxicity based on clinical signs, ophthalmic examinations, or laboratory results at any time point monitored in patients treated with up to 150 microgram/dose of POT- 4. Additionally, no serious adverse events and no identifiable intraocular inflammation were reported.

Preliminary results indicate that intravitreal POT-4 is safe, and the data accumulated so far support the continued investigation of POT-4 for the treatment of both dry and wet AMD with larger randomized clinical trials to further define its efficacy profile.

"These safety data strongly support the further development of POT-4 as a potential treatment for patients with AMD," said Cedric Francois, President and CEO of Potentia Pharmaceuticals. "We believe that the product has significant promise based on these early-stage findings and look forward to further testing of the compound in higher doses as we continue this trial."

About POT-4

POT-4 is a complement inhibitor, which shuts down the complement activation cascade that could otherwise lead to local inflammation, tissue damage and upregulation of angiogenic factors such as vascular endothelial growth factor (VEGF) in the eye. Based on this mechanism of action, POT-4 holds the potential to be effective against both dry and wet AMD.

About AMD

AMD is the leading cause of blindness in the elderly of the western world and affects more than 10 million patients in the United States alone. The current standard of care for AMD relies primarily on angiogenesis inhibitors, an approach geared towards the approximately 10-15% of AMD patients with complications resulting from ocular angiogenesis (growth of new blood vessels and bleeding in the back of the eye). No drug currently on the market has been approved for the treatment of the remaining patients, who suffer from the so- called "dry" form of the disease.

About the Complement System and POT-4

Complement activation is an inflammatory process involving dozens of plasma proteins, ultimately leading to cell membrane disruption through the membrane attack complex (MAC). Activation of the complement system is an important part of the body's defensive immune response against pathogens such as bacteria and viruses. In spite of its defensive function, inappropriate or excessive complement activation can have destructive consequences if left unchecked. Over the past three years, multiple scientific publications have strongly linked variants of genes encoding components of the complement system with a predisposition toward AMD.

POT-4 binds tightly to complement component C3, preventing its participation in the complement activation cascade. As C3 is the central component of all major complement activation pathways, its inhibition effectively shuts down downstream complement activation that could otherwise lead to local inflammation, tissue damage and upregulation of angiogenic factors such as vascular endothelial growth factors (VEGF).

About Potentia

Potentia Pharmaceuticals, Inc. is an early stage biotechnology company focused on developing novel therapeutics and drug delivery technologies to address chronic inflammatory diseases, with an initial emphasis on diseases of the eye such as age-related macular degeneration.

Media Requests:
Paul Kidwell
(617) 296-3854
paulkidwell@comcast.net

Contact for Potentia Pharmaceuticals:
Pascal Deschatelets
(502) 569-1053

SOURCE Potentia Pharmaceuticals, Inc.

 http://www.potentiapharma.com