Premium
Platelet mitochondrial activity and pesticide exposure in early Parkinson's disease
Author(s) -
Bronstein Jeff M.,
Paul Kimberly,
Yang Laurice,
Haas Richard H.,
Shults Clifford W.,
Le Thuy,
Ritz Beate
Publication year - 2015
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.26164
Subject(s) - parkinson's disease , nicotinamide adenine dinucleotide , mitochondrion , pesticide , case control study , pathogenesis , medicine , population , cohort , disease , biology , endocrinology , physiology , biochemistry , environmental health , enzyme , nad+ kinase , ecology
Background Mitochondrial dysfunction has been implicated in the pathogenesis of Parkinson's disease (PD), but the cause of this dysfunction is unclear. Methods Platelet 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. Results In 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. Conclusions Electron 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. © 2015 International Parkinson and Movement Disorder Society