Abnormalities of the electron transport chain in idiopathic parkinson's disease

Abnormalities of the electron transport chain in idiopathic parkinson's disease Idiopathic Parkinson's disease may have a low‐level familial association but does not follow mendelian patterns of inheritance. Since inheritance of some components of the electron transport chain is nonmendelian and since inhibition of the electron transport chain with the toxin 1‐methy1‐4‐phenyl‐1,2,3,6‐tetrahydropyridine models Parkinson's disease in humans and animals, we evaluated catalytic activities of the electron transport chain in platelet mitochondria purified from patients with idiopathic Parkinson's disease. All 10 patients studied had significant reductions of complex I (NADH:ubiquinone oxidoreductase) activity. Succinate:cytochrome c oxidoreductase activity was less strikingly reduced. We hypothesize that the complex I abnormality may have an etiological role in the pathogenesis of Parkinson's disease and that this defect may be derived via the mitochondrial genome. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Abnormalities of the electron transport chain in idiopathic parkinson's disease

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Publisher
Wiley
Copyright
Copyright © 1989 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.410260606
Publisher site
See Article on Publisher Site

Abstract

Idiopathic Parkinson's disease may have a low‐level familial association but does not follow mendelian patterns of inheritance. Since inheritance of some components of the electron transport chain is nonmendelian and since inhibition of the electron transport chain with the toxin 1‐methy1‐4‐phenyl‐1,2,3,6‐tetrahydropyridine models Parkinson's disease in humans and animals, we evaluated catalytic activities of the electron transport chain in platelet mitochondria purified from patients with idiopathic Parkinson's disease. All 10 patients studied had significant reductions of complex I (NADH:ubiquinone oxidoreductase) activity. Succinate:cytochrome c oxidoreductase activity was less strikingly reduced. We hypothesize that the complex I abnormality may have an etiological role in the pathogenesis of Parkinson's disease and that this defect may be derived via the mitochondrial genome.

Journal

Annals of NeurologyWiley

Published: Dec 1, 1989

References

  • Maternally inherited mitochondrial myopathy and myoclonic epilepsy
    Rosing, Rosing; Hopkins, Hopkins; Wallace, Wallace
  • A clinical survey of parkinsonism in Iceland
    Gudmundsson, Gudmundsson
  • Twin study of Parkinson disease
    Duvoisin, Duvoisin; Roswell, Roswell; Williams, Williams
  • Monozygotic twins with Parkinson's disease
    Koller, Koller; ; Hara, Hara; Nutt, Nutt
  • Parkinson's disease in monozygotic twins
    Jankovic, Jankovic; Reches, Reches
  • Parkinson's disease. A genetic study
    Martin, Martin; Young, Young; Anderson, Anderson

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