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May 2014

Targeting Mitochondria for Neuroprotection in Parkinson Disease

Author Affiliations
  • 1Department of Clinical Neurosciences, Institute of Neurology, University College London, London, England
  • 2Department of Cell and Developmental Biology, University College London, London, England
JAMA Neurol. 2014;71(5):537-538. doi:10.1001/jamaneurol.2014.64

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

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