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Major new finding on genetics of Parkinson's disease zeroes in on activity of alpha synuclein

Scientists investigating a rare familial form of early-onset Parkinson's disease have discovered that too much of a normal form of the -synuclein gene may cause Parkinson's disease. The finding, reported in the October 31, 2003, issue of Science, shows that abnormal multiplication of the -synuclein gene can cause the disease.

The study provides major new clues into the process by which Parkinson's disease develops. Further, it suggests another way of looking at the consequences of abnormal protein deposition in a variety of neurological diseases, such as Alzheimer's disease.

The Science findings are the product of collaboration among scientists at several institutions, including researchers at the National Institutes of Health (NIH), part of the U.S. Department of Health and Human Services. They were reported by Andrew Singleton, Ph.D., and colleagues at the National Institute on Aging's (NIA) Laboratory of Neurogenetics, Matthew Farrer, Ph.D., of the Mayo Clinic, and Katrina Gwinn-Hardy, M.D., of the National Institute of Neurological Disorders and Stroke (NINDS). The team also included scientists from the National Human Genome Research Institute (NHGRI) and Georgetown University Medical Center, Washington, DC.

Until very recently, researchers focused on possible environmental factors as the culprit in Parkinson's disease. However, in 1996, mutations in the -synuclein gene were identified in a few large families in whom the disease was unusually common. Since then, mutations in several other genes have also been linked to familial forms of Parkinson's disease.

In this new study, investigators analyzed blood samples from another affected family, the "Iowa kindred," in which many relatives developed Parkinson's disease or related neurological diseases. The family, followed by this team of researchers for many years, presented a puzzle to scientists because the genetic analyses of some family members initially show
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Contact: Vicky Cahan
cahanv@nia.nih.gov
301-496-1752
NIH/National Institute on Aging
30-Oct-2003


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