期刊
MOVEMENT DISORDERS
卷 30, 期 6, 页码 862-866出版社
WILEY-BLACKWELL
DOI: 10.1002/mds.26164
关键词
electron transport chain; complex I
资金
- Mitchell Foundation
- National Institute of Environmental Health Sciences (NIEHS) [P01ES016732, R01ES010544, 5R21ES16446-2, U54ES012078]
BackgroundMitochondrial dysfunction has been implicated in the pathogenesis of Parkinson's disease (PD), but the cause of this dysfunction is unclear. MethodsPlatelet mitochondrial complex I and I/III (nicotinamide adenine dinucleotide cytochrome c reductase, NCCR) activities were measured in early PD patients and matched controls enrolled in a population-based case-control study. Ambient agricultural pesticide exposures were assessed with a geographic information system and California Pesticide Use Registry. ResultsIn contrast to some previous reports, we found no differences in complex I and I/III activities in subjects with PD and controls. We did find that NCCR activity correlated with subjects' exposure to pesticides known to inhibit mitochondrial activity regardless of their diagnosis. ConclusionsElectron transport chain (ETC) activity is not altered in PD in this well-characterized cohort when compared with community-matched controls but appears to be affected by environmental toxins, such as mitochondria-inhibiting pesticides. (c) 2015 International Parkinson and Movement Disorder Society
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