| Literature DB >> 14642269 |
Jason L Eriksen1, Ted M Dawson, Dennis W Dickson, Leonard Petrucelli.
Abstract
Previous reports on Parkinson's disease indicate that genetic mutations in alpha-synuclein result in the aberrant accumulation of this protein, causing toxic gain of function leading to the development of Parkinson's. A recent report on the Iowan kindred, an extended pedigree with an autosomal dominant form of this disease, provides new mechanistic insight into Parkinson's disease by showing that an elevation in wild-type alpha-synuclein protein is sufficient to develop the early-onset form of the disorder. This review discusses how insights gained from these studies of alpha-synuclein may direct future research into Parkinson's disease.Entities:
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Year: 2003 PMID: 14642269 DOI: 10.1016/s0896-6273(03)00684-6
Source DB: PubMed Journal: Neuron ISSN: 0896-6273 Impact factor: 17.173