Mitochondrial dysfunction and oxidative stress in Parkinson's disease

Neurochem Res. 2008 Mar;33(3):589-97. doi: 10.1007/s11064-007-9482-y. Epub 2007 Oct 17.


Environmental toxins, genetic predisposition and old age are major risk factors for Parkinson's disease (PD). Although the mechanism(s) underlying selective dopaminergic (DA) neurodegeneration remain unclear, molecular studies in both toxin based models and genetic based models of the disease suggest a major etiologic role for mitochondrial dysfunction in the pathogenesis of PD. Further, recent studies have presented clear evidence for a high burden of mtDNA deletions within the substantia nigra neurons in individuals with PD. Ultimately, an understanding of the molecular events which precipitate DA neurodegeneration in idiopathic PD will enable the development of targeted and effective therapeutic strategies. We review recent advances and current understanding of the genetic factors, molecular mechanisms and animal models of PD.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA, Mitochondrial / drug effects
  • DNA, Mitochondrial / genetics
  • Disease Models, Animal
  • Humans
  • Inflammation / pathology
  • Mitochondrial Diseases / genetics
  • Mitochondrial Diseases / metabolism*
  • Mitochondrial Diseases / pathology*
  • Oxidative Stress / genetics
  • Oxidative Stress / physiology*
  • Parkinson Disease / genetics
  • Parkinson Disease / metabolism*
  • Parkinson Disease / pathology*
  • Proteasome Endopeptidase Complex / drug effects
  • Proteasome Endopeptidase Complex / metabolism
  • Signal Transduction / drug effects


  • DNA, Mitochondrial
  • Proteasome Endopeptidase Complex