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[ Eventual Huntington's Drug May Have Clear Path To Affected Brain Region, Solomon Snyder Tells Pharmacy Students ]

Eventual Huntington's Drug May Have Clear Path To Affected Brain Region, Solomon Snyder Tells Pharmacy Students

If a drug was developed to block a key protein linked to the onset of Huntington's Disease, it could have a clear path to the part of the brain most affected by the disease, while not bothering other parts of the brain and body, said distinguished neuroscientist Solomon H. Snyder, MD, to an audience of about 300 students and faculty at the University of Maryland, Baltimore (UMB). Snyder said, "Even though there is a market out there of only 100, 000 patients, " his laboratory at Johns Hopkins University is currently partnering with big pharmaceutical companies to develop such a drug, one to block binding of the Rhes protein to mutant huntingtin protein, a genetically altered protein in Huntington's Disease which kills cells in the brain's corpus striatum. Snyder presented the annual Ellis S.

Protecting The Brain From A Deadly Genetic Disease

Huntington's disease (HD) is a cruel, hereditary condition that leads to severe physical and mental deterioration, psychiatric problems and eventually, death. Currently, there are no treatments to slow down or stop it. HD sufferers are born with the disease although they do not show symptoms until late in life. In a new study published in The Journal of Neuroscience, Stephen Ferguson and Fabiola Ribeiro of Robarts Research Institute at The University of Western Ontario identified a protective pathway in the brain that may explain why HD symptoms take so long to appear. The findings could also lead to new treatments for HD. The symptoms of Huntington's disease are caused by cell death in specific regions of the brain. Patients who have HD are born with a mutated version of the protein huntingtin (Htt), which is thought to cause these toxic effects.

Long-Term Efficacy Of Xenazine reg; Tetrabenazine For The Treatment Of Chorea Associated With Huntington's Disease

Lundbeck Inc. has announced the presentation of results from an open-label extension study of Xenazine ® (tetrabenazine) for the treatment of chorea associated with Huntington's disease (HD). Data from this study demonstrated that after an 80-week treatment period, subjects treated with Xenazine experienced a statistically significant reduction in chorea score (p These results are consistent with the reduction in chorea score observed in a pivotal Phase 3 randomized, double-blind, placebo-controlled multi-center clinical study in which subjects were treated with Xenazine for 12 weeks.2 Data from the open-label study were presented at the 12th Annual American Society of Experimental NeuroTherapeutics (ASENT) meeting in Bethesda, Maryland (Poster No. 0029). Results of this study are published in BMC Neurology, an online open access journal at http://www.

Faulty Clean-up Process May Be Key Event In Huntington's Disease

In a step towards a possible treatment for Huntington's disease, scientists at Albert Einstein College of Medicine of Yeshiva University have shown for the first time that the accumulation of a mutated protein may explain damaging cellular behavior in Huntington's disease. Their research is described in the April 11 online edition of Nature Neuroscience. Huntington's disease, which afflicted the folksinger Woody Guthrie, is a fatal, inherited neurodegenerative disorder. While subtle personality changes and diminished physical skills may occur early in the disease, it typically becomes noticeable during middle age. Later problems include dementia and chorea - jerky movements that are random and uncontrollable. Huntington's disease results from a gene mutation that leads to a defective form of the huntingtin protein.

Huntington's Disease: Faulty Cleanup Process May Be Key Event In Cause

In a step towards a possible treatment for Huntington's disease, scientists at Albert Einstein College of Medicine of Yeshiva University have shown for the first time that the accumulation of a mutated protein may explain damaging cellular behavior in Huntington's disease. Their research is described in the April 11 online edition of Nature Neuroscience. Huntington's disease, which afflicted the folksinger Woody Guthrie, is a fatal, inherited neurodegenerative disorder. While subtle personality changes and diminished physical skills may occur early in the disease, it typically becomes noticeable during middle age. Later problems include dementia and chorea - jerky movements that are random and uncontrollable. Huntington's disease results from a gene mutation that leads to a defective form of the huntingtin protein.

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