Preventions of Eye

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

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

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

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

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

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

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

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

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?

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

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

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

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

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

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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!

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

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

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)

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

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

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

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

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

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

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

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

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)

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

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

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

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

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.