Caught in the act:: α-synuclein is the culprit in Parkinson's disease

被引：127

作者：

Eriksen, JL

Dawson, TM

Dickson, DW

Petrucelli, L

机构：

[1] Mayo Clin Jacksonville, Dept Neurogenet, Jacksonville, FL 32224 USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurol & Neurosci, Baltimore, MD 21287 USA

来源：

NEURON | 2003年 / 40卷 / 03期

关键词：

D O I：

10.1016/S0896-6273(03)00684-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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 wildtype 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.

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收藏

页码：453 / 456

页数：4

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