Researchers at the American Academy of Ophthalmology have found that Leber’s congenital Amaurosis (LCA), a very severe form of retinal disease
can be improved with the help of gene therapy.
Not only that, but the improvements were also found to be stable for two years.
Gene Therapy Can Correct Retinal Eye Diseases: LCA can be diagnosed in children at a very early age, sometimes even at infancy.
The main symptoms
of LCA are severity in vision loss and nystagmus(involuntary eye movement). By the time a person reaches his thirties or forties LCA develops into blindness.
* The impact of gene therapy could mainly be observed in children. The visual acuity and light sensitivity was tremendous in these children.
* Not only in children, researchers were also able to observe improvement in adults.
The Research and Theory: LCA is due to the mutations caused in any of the 13 genes in our body. Researchers were studying a Type 2 LCA which is due to mutation in the RPE65 gene.
* The doctors injected a normal functioning RPE65 gene which was joined with a virus into the sub-retinal space upon performing a surgery.
* The altered virus places the normally functioning RPE65 gene into the diseased cells and modifies the defective enzymes.
* After 2 weeks from the date of surgery, doctors observed that the patients reported an improvement in vision even in dim light.
* There were a few patients who also said that their visual acuity improved.
* A few even experienced massive improvement in nystagmus.
* The most encouraging result was that none of the patients experienced adverse effects.
Gene therapy does not improve sight on a permanent basis. But, gene therapy can correct inherited retinal eye diseases and help people restore sight.
People who undergo gene therapy need not be classified as blind any more. Researchers are trying hard to implement this technique in a safer way in younger children.
Monday, August 23, 2010
Wednesday, August 18, 2010
Drug Research could lead to AMD therapy
By Adrian Galbreth
New drug research may pave the way for more effective treatments of age-related macular degeneration - the leading cause of blindness in the western world.
Those are the claims being made by researchers at Tufts University School of Medicine, who say that a protein known as galectin-3 promotes the growth of new blood vessels, and that targeting the protein can "significantly reduce" angiogenesis.
The findings have been published in the Journal of Experimental Medicine and may lead to treatments for diseases caused by excessive angiogenesis, which include AMD, said Dr Noorjahan Panjwani, who led the project.
She explained: "Our study shows that galectin-3 protein binds to glycans of specific cell-adhesion proteins to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis."
Meanwhile, another team of researchers at Tufts have found that that non-viral gene therapy can delay the onset of some forms of eye disease and offer hope to retinal degeneration sufferers.ADNFCR-1853-ID-800028486-ADNFCR
New drug research may pave the way for more effective treatments of age-related macular degeneration - the leading cause of blindness in the western world.
Those are the claims being made by researchers at Tufts University School of Medicine, who say that a protein known as galectin-3 promotes the growth of new blood vessels, and that targeting the protein can "significantly reduce" angiogenesis.
The findings have been published in the Journal of Experimental Medicine and may lead to treatments for diseases caused by excessive angiogenesis, which include AMD, said Dr Noorjahan Panjwani, who led the project.
She explained: "Our study shows that galectin-3 protein binds to glycans of specific cell-adhesion proteins to activate the signaling pathways that bring about angiogenesis. This improved understanding may provide a more targeted approach to preventing harmful angiogenesis."
Meanwhile, another team of researchers at Tufts have found that that non-viral gene therapy can delay the onset of some forms of eye disease and offer hope to retinal degeneration sufferers.ADNFCR-1853-ID-800028486-ADNFCR
Wednesday, August 4, 2010
Visudyne therapy
Age-related macular degeneration (AMD) is a progressive disease of the eye, meaning that it can’t be cured. The good news is that AMD can be controlled. Treatments available today can slow the vision loss associated with AMD and even restore some vision.
Wet and dry age-related macular degeneration (AMD) differ in several important respects, including treatment options. The only way to find out which AMD treatment regimen or management plan is right for you is to talk to your ophthalmologist or retinal specialist.
Visudyne therapy treats a form of AMD called predominantly classic subfoveal CNV due to AMD.
In this form of AMD, abnormal blood vessels leak fluid and/or blood under the macula—the part of the eye responsible for central vision—causing serious vision loss. During therapy, Visudyne is injected into the patient (generally through the arm). Next, light from a low-energy laser activates Visudyne, causing it to destroy the leaky vessels. As a part of a wet AMD treatment regimen, Visudyne therapy may help slow its progression.
Ask your ophthalmologist or retinal specialist if Visudyne therapy may be right for you.
Other treatment options
Anti-VEGF (anti-vascular endothelial growth factor) treatments block the formation of new abnormal blood vessels
Wet and dry age-related macular degeneration (AMD) differ in several important respects, including treatment options. The only way to find out which AMD treatment regimen or management plan is right for you is to talk to your ophthalmologist or retinal specialist.
Visudyne therapy treats a form of AMD called predominantly classic subfoveal CNV due to AMD.
In this form of AMD, abnormal blood vessels leak fluid and/or blood under the macula—the part of the eye responsible for central vision—causing serious vision loss. During therapy, Visudyne is injected into the patient (generally through the arm). Next, light from a low-energy laser activates Visudyne, causing it to destroy the leaky vessels. As a part of a wet AMD treatment regimen, Visudyne therapy may help slow its progression.
Ask your ophthalmologist or retinal specialist if Visudyne therapy may be right for you.
Other treatment options
Anti-VEGF (anti-vascular endothelial growth factor) treatments block the formation of new abnormal blood vessels
Tuesday, July 27, 2010
Medicine from Moss to produce human protien
Diabetics use human insulin produced in bacteria in order to treat their metabolic disorder. Many other genetically engineered proteins are also on the advance. They are being used for diagnosis as well as for therapy.
Whereas insulin used to be extracted from slaughterhouse waste, today it is produced genetically in bacteria. However, more complex proteins have to be synthesised in more complex organisms. This takes place mostly in bioreactors using animal cell lines. Biotechnologist Prof. Ralf Reski from Freiburg, Germany, has developed the moss Physcomitrella patens into a safe and inexpensive alternative supplier of medicine.
His group has now, under Dr. Eva Decker, for the first time succeeded in producing a human protein in a moss bioreactor, which has been assigned the "orphan drug" status by the respective EU authorities. This means the development and approval of such medication receive particular support from the authorities. In many people the amount of this protein decreases with old age - with severe consequences. Eva Decker explains: "With the complement factor H we have produced a protein in moss that otherwise occurs only in blood and is important for the immune system. Not enough of this protein in older people is the main cause of blindness for 50 million people worldwide. This age-related macular degeneration (AMD) is a problem, particularly in industrialised countries."
Biochemists from the Freiburg Centre for Systems Biology under Dr. Andreas Schlosser were able to show with the help of high-performance mass spectrometers that the human factor H engineered into and produced by moss was a complete protein. Infection biologists headed by Prof. Peter F. Zipfel from the Hans-Knöll-Institute in Jena, Germany, were able to prove in biological assays that factor H from moss is fully functional. "Currently factor H is not available in pharmacies, so treatment for AMD with this protein is not possible. To date recombinant production of factor H was barely feasible. I am convinced that for the first time the moss bioreactor is a promising option", says Peter Zipfel.
This work was supported by the German Federal Ministry of Education and Research (BMBF), the Freiburg Initiative for Systems Biology and the Cluster of Excellence BIOSS.
Dr. Annette Büttner-Mainik, first author of the publication, was a Kekulé scholarship holder from the endowment fund of the German Chemical Industry (FCI).
The title of the original publication is: Annette Büttner-Mainik, Juliana Parsons, Hanna Jérôme, Andrea Hartmann, Stephanie Lamer, Andreas Schaaf, Andreas Schlosser, Peter F. Zipfel, Ralf Reski, Eva L. Decker (2010): Production of biologically active recombinant human Factor H in Physcomitrella. Plant Biotechnology Journal, doi: 10.1111/j.1467-7652.2010.00552.x.
"It will take a while before medication produced in moss is available in pharmacies", says Ralf Reski, member of the Innovation Think Tank of the governor of Baden-Wuerttemberg. "We are further optimising the moss bioreactor using methods from Systems Biology and Synthetic Biology. However, the implementation of clinical studies and the setting up of industrial production is long-winded and expensive; this is the task of industry and not of university research."
Whereas insulin used to be extracted from slaughterhouse waste, today it is produced genetically in bacteria. However, more complex proteins have to be synthesised in more complex organisms. This takes place mostly in bioreactors using animal cell lines. Biotechnologist Prof. Ralf Reski from Freiburg, Germany, has developed the moss Physcomitrella patens into a safe and inexpensive alternative supplier of medicine.
His group has now, under Dr. Eva Decker, for the first time succeeded in producing a human protein in a moss bioreactor, which has been assigned the "orphan drug" status by the respective EU authorities. This means the development and approval of such medication receive particular support from the authorities. In many people the amount of this protein decreases with old age - with severe consequences. Eva Decker explains: "With the complement factor H we have produced a protein in moss that otherwise occurs only in blood and is important for the immune system. Not enough of this protein in older people is the main cause of blindness for 50 million people worldwide. This age-related macular degeneration (AMD) is a problem, particularly in industrialised countries."
Biochemists from the Freiburg Centre for Systems Biology under Dr. Andreas Schlosser were able to show with the help of high-performance mass spectrometers that the human factor H engineered into and produced by moss was a complete protein. Infection biologists headed by Prof. Peter F. Zipfel from the Hans-Knöll-Institute in Jena, Germany, were able to prove in biological assays that factor H from moss is fully functional. "Currently factor H is not available in pharmacies, so treatment for AMD with this protein is not possible. To date recombinant production of factor H was barely feasible. I am convinced that for the first time the moss bioreactor is a promising option", says Peter Zipfel.
This work was supported by the German Federal Ministry of Education and Research (BMBF), the Freiburg Initiative for Systems Biology and the Cluster of Excellence BIOSS.
Dr. Annette Büttner-Mainik, first author of the publication, was a Kekulé scholarship holder from the endowment fund of the German Chemical Industry (FCI).
The title of the original publication is: Annette Büttner-Mainik, Juliana Parsons, Hanna Jérôme, Andrea Hartmann, Stephanie Lamer, Andreas Schaaf, Andreas Schlosser, Peter F. Zipfel, Ralf Reski, Eva L. Decker (2010): Production of biologically active recombinant human Factor H in Physcomitrella. Plant Biotechnology Journal, doi: 10.1111/j.1467-7652.2010.00552.x.
"It will take a while before medication produced in moss is available in pharmacies", says Ralf Reski, member of the Innovation Think Tank of the governor of Baden-Wuerttemberg. "We are further optimising the moss bioreactor using methods from Systems Biology and Synthetic Biology. However, the implementation of clinical studies and the setting up of industrial production is long-winded and expensive; this is the task of industry and not of university research."
Tuesday, July 20, 2010
Stem Cell Transplants Stalled Blindness in Rats
Researchers say putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.Nerve stem cell transplants may help slow the progression of macular degeneration, the most common cause of blindness in the developed world, U.S. researchers said on Monday.
They said putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.
"These cells improve the chemical environment in the back of the eye," said Ray Lund of the Casey Eye Institute at Oregon Health & Science University in Portland, whose findings were presented at the Society for Neuroscience meeting in Chicago.
Lund said the mechanism is not clear, but he suspects that when immature nerve cells are placed near the retina, they produce growth factors that protect the cells from damage by the disease.
"It's basically a chemical pump that is sitting in the right place and producing the right things," Lund said in a telephone interview.
Where normally animals with eye disease lost their vision by three months old, rats that got the transplants kept their vision for at least seven months, he said.
"There is no evidence that they (the transplanted cells) do any damage," Lund said, adding that the animals do not develop tumors, a key worry for stem cell transplants.
The findings raise hope for use of the treatment in humans with a range of diseases in which the retina become damaged, including age-related macular degeneration or AMD, which affects nearly 30 million people worldwide, including 15 million Americans.
People with AMD lose central vision when delicate light-sensing cells of the macula, a region at the center of the retina, become damaged.
In the rats, the researchers transplanted immature nerve cells into the space near the retina. Lund said the same could be done in people with retinal disease.
Dr. Stephen Huhn, head of the Central Nervous System research program at StemCells Inc, said the cells are adult neural stem cells. He said they are multipotent, meaning they can morph into different types of nerve cells.
The company has already tested the treatment in a study of six patients with Batten's disease, a fatal inherited disorder of the nervous system.
"Having a cell that has already entered clinical testing that has been well tolerated at very high doses in the brain gives us a lot of confidence about exploring the same type of strategy in the eye," Huhn said.
Huhn said he thinks the cells may be especially well suited for use in the retina, brain and spinal cord, which are less likely to reject the cells than other parts of the body.
Ultimately, he said the hope is to develop a treatment for the dry form of macular degeneration, which affects around 90 percent of patients diagnosed with AMD. No treatments are available for this form of the disease.
Huhn said treating this form of the disease may prevent some people from developing wet AMD, in which tiny new blood vessels grow between the retina and the back of the eye.
This form of the disease can be treated with modern drugs like Lucentis, from Novartis and Roche's Genentech, and Pfizer's Macugen.
They said putting nerve stem cells from StemCells Inc near the retinas of rats with a form of macular degeneration helped keep the disease from advancing to blindness for several months.
"These cells improve the chemical environment in the back of the eye," said Ray Lund of the Casey Eye Institute at Oregon Health & Science University in Portland, whose findings were presented at the Society for Neuroscience meeting in Chicago.
Lund said the mechanism is not clear, but he suspects that when immature nerve cells are placed near the retina, they produce growth factors that protect the cells from damage by the disease.
"It's basically a chemical pump that is sitting in the right place and producing the right things," Lund said in a telephone interview.
Where normally animals with eye disease lost their vision by three months old, rats that got the transplants kept their vision for at least seven months, he said.
"There is no evidence that they (the transplanted cells) do any damage," Lund said, adding that the animals do not develop tumors, a key worry for stem cell transplants.
The findings raise hope for use of the treatment in humans with a range of diseases in which the retina become damaged, including age-related macular degeneration or AMD, which affects nearly 30 million people worldwide, including 15 million Americans.
People with AMD lose central vision when delicate light-sensing cells of the macula, a region at the center of the retina, become damaged.
In the rats, the researchers transplanted immature nerve cells into the space near the retina. Lund said the same could be done in people with retinal disease.
Dr. Stephen Huhn, head of the Central Nervous System research program at StemCells Inc, said the cells are adult neural stem cells. He said they are multipotent, meaning they can morph into different types of nerve cells.
The company has already tested the treatment in a study of six patients with Batten's disease, a fatal inherited disorder of the nervous system.
"Having a cell that has already entered clinical testing that has been well tolerated at very high doses in the brain gives us a lot of confidence about exploring the same type of strategy in the eye," Huhn said.
Huhn said he thinks the cells may be especially well suited for use in the retina, brain and spinal cord, which are less likely to reject the cells than other parts of the body.
Ultimately, he said the hope is to develop a treatment for the dry form of macular degeneration, which affects around 90 percent of patients diagnosed with AMD. No treatments are available for this form of the disease.
Huhn said treating this form of the disease may prevent some people from developing wet AMD, in which tiny new blood vessels grow between the retina and the back of the eye.
This form of the disease can be treated with modern drugs like Lucentis, from Novartis and Roche's Genentech, and Pfizer's Macugen.
Wednesday, June 30, 2010
Stem cell Therapy to Benefit Blind
Submitted by Jayden Roberts on Tue, 06/29/2010
Italian researchers have reported that about 12 people have regained their sight in a successful experiment conducted with some partly blind and severe eye damage suffering people. This was revealed in a study published online in the New England Journal of Medicine.
This is a remarkable success that will encourage the cell-therapy, which is done by transplanting cells from one’s own body to other parts. It has been claimed that the treatment has proved winning in 82 of 107 eyes. Also, it was partially complete in 14 others eyes. The benefits of the treatment are expected to last till 10 years after the process.
It is also noticeable that one man, who had been blind for more than five decades, have also completely restored his visual capacity. Appreciating the success, Ophthalmologist Ivan Schwab of the University of California praised and congratulated the team.
If the stem cell transplants become popular and are implemented even more, they can also prove helpful for the people who are affected by chemical burns on their corneas from heavy-duty cleansers and other chemicals. This will be a great help for people who have to suffer eyesight loss due to such mishaps.
However, the stem cell approach is not capable to treat optic nerve or macular degeneration, which is caused due to the damage in retina, as the treatment requires a few healthy tissues that can be transplanted.
Italian researchers have reported that about 12 people have regained their sight in a successful experiment conducted with some partly blind and severe eye damage suffering people. This was revealed in a study published online in the New England Journal of Medicine.
This is a remarkable success that will encourage the cell-therapy, which is done by transplanting cells from one’s own body to other parts. It has been claimed that the treatment has proved winning in 82 of 107 eyes. Also, it was partially complete in 14 others eyes. The benefits of the treatment are expected to last till 10 years after the process.
It is also noticeable that one man, who had been blind for more than five decades, have also completely restored his visual capacity. Appreciating the success, Ophthalmologist Ivan Schwab of the University of California praised and congratulated the team.
If the stem cell transplants become popular and are implemented even more, they can also prove helpful for the people who are affected by chemical burns on their corneas from heavy-duty cleansers and other chemicals. This will be a great help for people who have to suffer eyesight loss due to such mishaps.
However, the stem cell approach is not capable to treat optic nerve or macular degeneration, which is caused due to the damage in retina, as the treatment requires a few healthy tissues that can be transplanted.
Thursday, June 10, 2010
Ann Arbor Pharma Firm Testing Zinc For Alzheimer's Treatment
Ann Arbor-based Adeona Pharmaceuticals Inc. (AMEX: AEN) Monday announced the completion of 50 percnet enrollment in Part 2 of its clinical study, "A Prospective, Randomized, Double Blind Trial of a Novel Oral Zinc Cysteine Preparation in Alzheimer's Disease (CopperProof-2)."
The CopperProof-2 study represents the first controlled clinical study of oral zinc cysteine for the dietary management of Alzheimer's disease and mild cognitive impairment.
Part 2 of the CopperProof-2 study is designed as a 60-subject comparator study. Subjects are randomized on a 50:50 basis to receive either Zinthionein ZC or matching placebo. After 3 and 6 months on clinical trial material, serum measurements of zinc and copper are taken, and any changes in cognitive function using standard clinical tests used in Alzheimer's disease and mild cognitive impairment are recorded.
The completion of 50 percent enrollment follows Adeona's April 14 announcement of positive results from Part 1 of the CopperProof-2 study. Part 1 demonstrated a substantially lower incidence of adverse effects in Alzheimer's disease and mild cognitive impairment subjects (33 percent versus 100 percent) in favor of Zinthionein ZC (containing 150 mg of elemental zinc acetate and 100 mg of cysteine) compared to Galzin (containing either 50 mg or 100 mg of elemental zinc as zinc acetate).
Zinthionein ZC also demonstrated superior serum zinc bioavailability in Alzheimer's disease and mild cognitive impairment subjects compared to both the 50 mg and 100 mg dose levels of Galzin.
"Having pioneered the use of oral zinc therapy in dry age-related macular degeneration, which has now become the standard of care, I believe that Adeona's once-daily, high bioavailability, well-tolerated oral zinc cysteine formulation has the potential to ameliorate the sub-clinical zinc deficiency in Alzheimer's and mild cognitive impairment subjects and substantially grow current markets for oral zinc-based therapies," said David Newsome, M.D., Adeona's senior vice president for research and development.
Added Adeona CEO James S. Kuo, M.D.: "We are pleased to have reached this enrollment milestone on a timely basis and within budget. Along with the recently announced Meda collaboration for flupirtine's development and completion of 50 percent enrollment in the Trimesta multiple sclerosis clinical trial, it represents one of several major transformational changes taking place at the company in the past few months."
Observations by Adeona scientists and other scientists of sub-clinical zinc deficiency in Alzheimer's disease patients plus a body of published literature that chronic elevated copper exposure contributes to the progression of Alzheimer's disease and mild cognitive impairment prompted the present CopperProof-2 clinical study.
Alzheimer's disease can affect the entire brain but it is particularly associated with loss of tissue in the hippocampus, the area in the brain responsible for several functions including short-term memory retention and processing. The hippocampus has one of the highest concentrations of zinc in the brain. Hippocampal zinc is thought to play a role in hundreds of protective enzymes and other systems, including those that detoxify amyloid beta, an abnormally folded peptide that accumulates in aging and is a biomarker for Alzheimer's disease. When cerebrospinal fluid zinc is low, levels of the particularly toxic beta amyloid 42 are elevated.
Hippocampal zinc serves as a neurotransmitter, and also modulates a specific neuroreceptor. If the neuroexcitation goes uncontrolled, there is a derangement of brain tissue function, and possibly neuronal death. By elevating cerebrospinal fluid zinc, the receptor excitation may be better controlled, improving tissue function and thereby acute cognition and tissue survival, as may have been seen in the 1992 study. NMDA-receptor antagonists now available for Alzheimer's, including Namenda and Axura, annually sell an estimated $2.6 billion.
Zinthionein ZC is a once-daily, gastroretentive, sustained-release, oral tablet formulation of zinc and cysteine. Zinc, an essential nutrient, participates as a necessary factor in the activity of over 200 enzymes and the DNA binding capacity of over 400 nuclear regulatory elements. Zinc may also directly participate in antioxidant protection by reducing the susceptibility of sulfhydril groups to damage by oxidative free radicals. Cysteine is an amino acid that has potent anti-oxidant properties and is a necessary component of the copper-zinc-binding protein, metallothionein.
Zinthionein ZC was invented and developed by Adeona scientists to achieve the convenience of once-daily dosing, high oral bioavailability and to minimize gastrointestinal side effects associated with other commercially available, oral zinc products. All of Zinthionein ZC's constituents have GRAS (Generally Regarded as Safe) status. Adeona is developing Zinthionein ZC as a prescription medical food for the dietary management of Alzheimer's disease and mild cognitive impairment. Zinthionein ZC is protected by multiple U.S. and international pending patent applications held by Adeona.
Adeona is a pharmaceutical company developing new medicines for serious central nervous systems diseases. Adeona's primary strategy is to in-license clinical-stage drug candidates that have already demonstrated a certain level of clinical efficacy and develop them to an inflection point in valuation resulting in a significant development and marketing collaboration.
Its other drugs include Trimesta (estriol) is an investigational oral drug for the treatment of relapsing remitting multiple sclerosis, currently in clinical trials, and Effirma (flupirtine), a centrally-acting investigational oral drug for the treatment of fibromyalgia syndrome. Adeona has entered into a potential $17.5 million corporate partnership with Meda AB. As part of the agreement, Meda will assume all future development costs while Adeona is entitled to receive milestone payments and royalties.
The CopperProof-2 study represents the first controlled clinical study of oral zinc cysteine for the dietary management of Alzheimer's disease and mild cognitive impairment.
Part 2 of the CopperProof-2 study is designed as a 60-subject comparator study. Subjects are randomized on a 50:50 basis to receive either Zinthionein ZC or matching placebo. After 3 and 6 months on clinical trial material, serum measurements of zinc and copper are taken, and any changes in cognitive function using standard clinical tests used in Alzheimer's disease and mild cognitive impairment are recorded.
The completion of 50 percent enrollment follows Adeona's April 14 announcement of positive results from Part 1 of the CopperProof-2 study. Part 1 demonstrated a substantially lower incidence of adverse effects in Alzheimer's disease and mild cognitive impairment subjects (33 percent versus 100 percent) in favor of Zinthionein ZC (containing 150 mg of elemental zinc acetate and 100 mg of cysteine) compared to Galzin (containing either 50 mg or 100 mg of elemental zinc as zinc acetate).
Zinthionein ZC also demonstrated superior serum zinc bioavailability in Alzheimer's disease and mild cognitive impairment subjects compared to both the 50 mg and 100 mg dose levels of Galzin.
"Having pioneered the use of oral zinc therapy in dry age-related macular degeneration, which has now become the standard of care, I believe that Adeona's once-daily, high bioavailability, well-tolerated oral zinc cysteine formulation has the potential to ameliorate the sub-clinical zinc deficiency in Alzheimer's and mild cognitive impairment subjects and substantially grow current markets for oral zinc-based therapies," said David Newsome, M.D., Adeona's senior vice president for research and development.
Added Adeona CEO James S. Kuo, M.D.: "We are pleased to have reached this enrollment milestone on a timely basis and within budget. Along with the recently announced Meda collaboration for flupirtine's development and completion of 50 percent enrollment in the Trimesta multiple sclerosis clinical trial, it represents one of several major transformational changes taking place at the company in the past few months."
Observations by Adeona scientists and other scientists of sub-clinical zinc deficiency in Alzheimer's disease patients plus a body of published literature that chronic elevated copper exposure contributes to the progression of Alzheimer's disease and mild cognitive impairment prompted the present CopperProof-2 clinical study.
Alzheimer's disease can affect the entire brain but it is particularly associated with loss of tissue in the hippocampus, the area in the brain responsible for several functions including short-term memory retention and processing. The hippocampus has one of the highest concentrations of zinc in the brain. Hippocampal zinc is thought to play a role in hundreds of protective enzymes and other systems, including those that detoxify amyloid beta, an abnormally folded peptide that accumulates in aging and is a biomarker for Alzheimer's disease. When cerebrospinal fluid zinc is low, levels of the particularly toxic beta amyloid 42 are elevated.
Hippocampal zinc serves as a neurotransmitter, and also modulates a specific neuroreceptor. If the neuroexcitation goes uncontrolled, there is a derangement of brain tissue function, and possibly neuronal death. By elevating cerebrospinal fluid zinc, the receptor excitation may be better controlled, improving tissue function and thereby acute cognition and tissue survival, as may have been seen in the 1992 study. NMDA-receptor antagonists now available for Alzheimer's, including Namenda and Axura, annually sell an estimated $2.6 billion.
Zinthionein ZC is a once-daily, gastroretentive, sustained-release, oral tablet formulation of zinc and cysteine. Zinc, an essential nutrient, participates as a necessary factor in the activity of over 200 enzymes and the DNA binding capacity of over 400 nuclear regulatory elements. Zinc may also directly participate in antioxidant protection by reducing the susceptibility of sulfhydril groups to damage by oxidative free radicals. Cysteine is an amino acid that has potent anti-oxidant properties and is a necessary component of the copper-zinc-binding protein, metallothionein.
Zinthionein ZC was invented and developed by Adeona scientists to achieve the convenience of once-daily dosing, high oral bioavailability and to minimize gastrointestinal side effects associated with other commercially available, oral zinc products. All of Zinthionein ZC's constituents have GRAS (Generally Regarded as Safe) status. Adeona is developing Zinthionein ZC as a prescription medical food for the dietary management of Alzheimer's disease and mild cognitive impairment. Zinthionein ZC is protected by multiple U.S. and international pending patent applications held by Adeona.
Adeona is a pharmaceutical company developing new medicines for serious central nervous systems diseases. Adeona's primary strategy is to in-license clinical-stage drug candidates that have already demonstrated a certain level of clinical efficacy and develop them to an inflection point in valuation resulting in a significant development and marketing collaboration.
Its other drugs include Trimesta (estriol) is an investigational oral drug for the treatment of relapsing remitting multiple sclerosis, currently in clinical trials, and Effirma (flupirtine), a centrally-acting investigational oral drug for the treatment of fibromyalgia syndrome. Adeona has entered into a potential $17.5 million corporate partnership with Meda AB. As part of the agreement, Meda will assume all future development costs while Adeona is entitled to receive milestone payments and royalties.
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