Mitochondrial Polymorphisms Significantly Reduce the Risk of Parkinson Disease
Identifieur interne : 000003 ( Pmc/Corpus ); précédent : 000002; suivant : 000004Mitochondrial Polymorphisms Significantly Reduce the Risk of Parkinson Disease
Auteurs : Joelle Van ; Kristin Nicodemus ; Eden Martin ; William Scott ; Martha Nance ; Ray Watts ; Jean Hubble ; Jonathan Haines ; William Koller ; Kelly Lyons ; Rajesh Pahwa ; Matthew Stern ; Amy Colcher ; Bradley Hiner ; Joseph Jankovic ; William Ondo ; Fred Allen ; Christopher Goetz ; Gary Small ; Frank Mastaglia ; Jeffrey Stajich ; Adam Mclaurin ; Lefkos Middleton ; Burton Scott ; Donald Schmechel ; Margaret Pericak ; Jeffery VanceSource :
- American Journal of Human Genetics [ 0002-9297 ] ; 2003.
Abstract
Mitochondrial (mt) impairment, particularly within complex I of the electron transport system, has been implicated in the pathogenesis of Parkinson disease (PD). More than half of mitochondrially encoded polypeptides form part of the reduced nicotinamide adenine dinucleotide dehydrogenase (NADH) complex I enzyme. To test the hypothesis that mtDNA variation contributes to PD expression, we genotyped 10 single-nucleotide polymorphisms (SNPs) that define the European mtDNA haplogroups in 609 white patients with PD and 340 unaffected white control subjects. Overall, individuals classified as haplogroup J (odds ratio [OR] 0.55; 95% confidence interval [CI] 0.34–0.91;
Url:
PubMed: 12618962
PubMed Central: 1180345
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