Neurotoxicity and neuroprotection in Parkinson's disease.
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.
Lange
K W
KW
Department of Clinical Neurochemistry, University of Würzburg, Federal Republic of Germany.
Youdim
M B
MB
Riederer
P
P
D000978:Antiparkinson Agents / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007501:Iron / Q000378:metabolism; D008543:Melanins / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D009498:Neurotoxins / Q000378:metabolism; D010084:Oxidation-Reduction; D010300:Parkinson Disease / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D012642:Selegiline / Q000627:therapeutic use; D013378:Substantia Nigra / Q000378:metabolism
D000978:Antiparkinson Agents; D008543:Melanins; D009498:Neurotoxins; D012642:Selegiline; D007501:Iron; D005978:Glutathione