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Editorial |

Mitochondrial Therapy for Parkinson Disease

Roger N. Rosenberg, MD
Arch Neurol. 2002;59(10):1523. doi:10.1001/archneur.59.10.1523.
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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 the loss of dopamine and dopaminergic axons in the striatum in 1-year-old mice treated with MPTP.

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