Caught in the act: alpha-synuclein is the culprit in Parkinson's disease.
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.
Eriksen
Jason L
JL
Department of Neurogenetics, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA.
Dawson
Ted M
TM
Dickson
Dennis W
DW
Petrucelli
Leonard
L
D000818:Animals; D001921:Brain / Q000033:anatomy & histology / Q000378:metabolism / Q000473:pathology; D005799:Genes, Dominant; D006801:Humans; D016631:Lewy Bodies / Q000378:metabolism / Q000473:pathology; D009410:Nerve Degeneration / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D010300:Parkinson Disease / Q000378:metabolism* / Q000473:pathology; D020543:Proteome / Q000378:metabolism; D051843:Synucleins; D051844:alpha-Synuclein
D009419:Nerve Tissue Proteins; D020543:Proteome; C497604:SNCA protein, human; D051843:Synucleins; D051844:alpha-Synuclein