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 in | Movement disorders Vol. 30; no. 6; pp. 862 - 866 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.05.2015
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 0885-3185 1531-8257 1531-8257 |
DOI | 10.1002/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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Bibliography: | istex:7134C2F6C407CAA289960FC8ECDB64DEEE047D12 ArticleID:MDS26164 ark:/67375/WNG-B3X4BKPQ-W 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). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0885-3185 1531-8257 1531-8257 |
DOI: | 10.1002/mds.26164 |