Abnormalities of the electron transport chain in idiopathic parkinson's disease
Corresponding Author
Dr William Davis Parker Jr MD
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Department of Pediatrics, University of Colorado School of Medicine, Denver, CO
Section of Pediatric Neurology, Box C-233, University of Colorado Health Sciences Center, Denver, CO 80262Search for more papers by this authorSally J. Boyson MD
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Search for more papers by this authorJanice K. Parks BA
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Search for more papers by this authorCorresponding Author
Dr William Davis Parker Jr MD
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Department of Pediatrics, University of Colorado School of Medicine, Denver, CO
Section of Pediatric Neurology, Box C-233, University of Colorado Health Sciences Center, Denver, CO 80262Search for more papers by this authorSally J. Boyson MD
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Search for more papers by this authorJanice K. Parks BA
Department of Neurology, University of Colorado School of Medicine, Denver, CO
Search for more papers by this authorAbstract
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.
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