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

Jason L. Eriksen, Ted M. Dawson, Dennis W. Dickson, Leonard Petrucelli

Research output: Contribution to journalReview article

Abstract

Previous reports on Parkinson's disease indicate that genetic mutations in α-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 α-synuclein protein is sufficient to develop the early-onset form of the disorder. This review discusses how insights gained from these studies of α-synuclein may direct future research into Parkinson's disease.

Original languageEnglish (US)
Pages (from-to)453-456
Number of pages4
JournalNeuron
Volume40
Issue number3
DOIs
StatePublished - Oct 30 2003

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ASJC Scopus subject areas

  • Neuroscience(all)

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