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Parkinson disease (PD) has been strongly associated with systemic defects in mitochondrial function. The best characterized of these is probably reduced activity of complex I of the electron transport chain, which was first reported more than 25 years ago,1 after the discovery of the pro-parkinsonian toxin, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), and its mechanism of action: inhibition of complex I.2 Proof-of-concept that a systemic impairment of complex I can reproduce the selective nigrostriatal degeneration and Lewy pathology of PD came from the rotenone model of PD in rats in 2000.3 Shortly thereafter, it became clear that certain autosomal recessive forms of PD are caused by mutations in genes that affect mitochondrial function or quality control, such as parkin and PINK1. Moreover, both parkin and PINK1 mutations are associated with a loss of complex I activity.4,5
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