Platelet mitochondrial activity and pesticide exposure in early Parkinson's disease

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...

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Published inMovement disorders Vol. 30; no. 6; pp. 862 - 866
Main Authors Bronstein, Jeff M., Paul, Kimberly, Yang, Laurice, Haas, Richard H., Shults, Clifford W., Le, Thuy, Ritz, Beate
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.05.2015
Wiley Subscription Services, Inc
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ISSN0885-3185
1531-8257
1531-8257
DOI10.1002/mds.26164

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Summary: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
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ArticleID:MDS26164
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Deceased.
Dr. Bronstein received support from the Veterans Administration Healthcare System (SW PADRECC), the Levine Foundation, and the Parkinson Alliance. Dr. Haas was supported by the Wright Family Foundation and NINDS (R01NS036714). The authors have no other relevant affiliations or financial involvement with any organization which would pose a conflict with the subject matter discussed in this manuscript.
Relevant conflicts of interest/financial disclosures
Author roles may be found in the online version of this article.
Funding agencies
This work was supported by the Mitchell Foundation and in part by the National Institute of Environmental Health Sciences (NIEHS Grants P01ES016732, R01ES010544, 5R21ES16446‐2, and U54ES012078).
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ISSN:0885-3185
1531-8257
1531-8257
DOI:10.1002/mds.26164