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Arch Neurol. 2002;59:1523.

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THE PRECISE causes of Parkinson disease (PD) are beginning to be defined and include specific genetic mutations causal of autosomal dominant (alpha-synuclein mutations) and recessive (Parkin mutations) phenotypes and for sporadic PD, an interaction between genetic and environmental factors.^1-2 An important emerging molecular defect is impaired function of the mitochondrial electron transport chain, particularly inhibition of complexes I and II/III, leading to failure of adenosine triphosphate synthesis. Inhibition of complex I by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) can cause human parkinsonism.^3-4 Schapira and colleagues⁵ have found a selective decrease in complex I activity in postmortem PD substantia nigra but not in patients with multiple system atrophy. Untreated PD patients have reduced activity of complexes I and II/III in mitochondria isolated from platelets.⁶ Shults et al⁷ have demonstrated reduced levels of coenzyme Q₁₀ in the mitochondria from platelets isolated from PD patients. Beal et al⁸ have shown that oral supplementation with coenzyme Q₁₀ reduced . . . [Full Text of this Article]