作者: Jason L Eriksen , Ted M Dawson , Dennis W Dickson , Leonard Petrucelli
DOI: 10.1016/S0896-6273(03)00684-6
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摘要: Abstract Previous reports on Parkinson's disease indicate that genetic mutations in α-synuclein result the aberrant accumulation of this protein, causing toxic gain function leading to development Parkinson's. A recent report Iowan kindred, an extended pedigree with autosomal dominant form disease, provides new mechanistic insight into by showing elevation wild-type protein is sufficient develop early-onset disorder. This review discusses how insights gained from these studies may direct future research disease.