Abstract
The etiology of sporadic Parkinson's disease (PD) is unknown, although mitochondrial dysfunction and oxidative stress have been implicated in the mechanisms associated with PD pathogenesis. Dopamine (DA) neurons of the substantia nigra pars compacta have been shown to degenerate to a greater extent in PD than other neurons suggesting the possibility that DA itself may be contributing to the neurodegenerative process. This review discusses our work on the effects of DA oxidation and reactive DA quinones on mitochondrial function and protein modification and the potential for exacerbating toxicity associated with mitochondrial dysfunction in PD.
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