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Abnormalities of the electron transport chain in idiopathic parkinson's disease
Author(s) -
Parker William Davis,
Boyson Sally J.,
Parks Janice K.
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410260606
Subject(s) - parkinson's disease , mitochondrion , disease , electron transport chain , pathogenesis , oxidoreductase , abnormality , etiology , medicine , chemistry , biology , biochemistry , enzyme , psychiatry
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.