Neurotoxicity and neuroprotection in Parkinson's disease

J Neural Transm Suppl. 1992:38:27-44.

Abstract

Recent findings of impaired mitochondrial function, altered iron metabolism and increased lipid peroxidation in the substantia nigra in Parkinson's disease emphasize the significance of oxidative stress and free radical formation in the pathogenesis of the disease. Future research will focus on improvements in neuroprotective therapy to prevent or slow the rate of progression of Parkinson's disease. Possible neuroprotective strategies include free radical scavengers, monoamine oxidase-B inhibitors, iron chelators and glutamate antagonists.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antiparkinson Agents / therapeutic use*
  • Glutathione / metabolism
  • Humans
  • Iron / metabolism
  • Melanins / metabolism
  • Mitochondria / metabolism
  • Neurotoxins / metabolism
  • Oxidation-Reduction
  • Parkinson Disease / drug therapy
  • Parkinson Disease / etiology
  • Parkinson Disease / metabolism*
  • Selegiline / therapeutic use
  • Substantia Nigra / metabolism

Substances

  • Antiparkinson Agents
  • Melanins
  • Neurotoxins
  • Selegiline
  • Iron
  • Glutathione