It is now generally accepted that mitochondrial dysfunction plays a significant role in the etiology and pathogenesis of Parkinson disease (PD). Mitochondrial involvement in PD was first identified with specific defects of mitochondrial complex I of the respiratory chain in substantia nigra,1,2 and abnormalities of this protein in the brain of individuals with PD have been identified in additional studies of protein expression.3 Significant support for the mitochondrial theory of PD causation has come from the discovery of mutations of mitochondrial proteins as a cause for parkinsonism (eg, PINK1, parkin, and DJ1).4
Schapira AHV, Patel S. Targeting Mitochondria for Neuroprotection in Parkinson Disease. JAMA Neurol. 2014;71(5):537–538. doi:https://doi.org/10.1001/jamaneurol.2014.64
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