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Neurobiol Dis. 2013 Mar;51:35-42. doi: 10.1016/j.nbd.2012.10.011. Epub 2012 Oct 12.

Mitochondrial dysfunction and oxidative stress in Parkinson's disease and monogenic parkinsonism.

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Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.


The pathogenic mechanisms that underlie Parkinson's disease remain unknown. Here, we review evidence from both sporadic and genetic forms of Parkinson's disease that implicate both mitochondria and oxidative stress as central players in disease pathogenesis. A systemic deficiency in complex I of the mitochondrial electron transport chain is evident in many patients with the disease. Oxidative stress caused by reactive metabolites of dopamine and alterations in the levels of iron and glutathione in the substantia nigra accompany this mitochondrial dysfunction. Recent evidence from studies on the genetic forms of parkinsonism with particular stress on DJ-1, parkin, and PINK-1 also suggest the involvement of mitochondria and oxidative stress.

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