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

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

doi:10.1016/S0896-6273(03)00684-6

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

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

Neuroscience

Research output: Contribution to journal › Review article › peer-review

132 Scopus citations

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 language	English (US)
Pages (from-to)	453-456
Number of pages	4
Journal	Neuron
Volume	40
Issue number	3
DOIs	https://doi.org/10.1016/S0896-6273(03)00684-6
State	Published - Oct 30 2003

ASJC Scopus subject areas

Neuroscience(all)

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title = "Caught in the act: α-synuclein is the culprit in Parkinson's disease",

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.",

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AU - Dawson, Ted M.

AU - Dickson, Dennis W.

AU - Petrucelli, Leonard

PY - 2003/10/30

Y1 - 2003/10/30

N2 - 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.

AB - 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.

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

Abstract

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