Neuroprotection by anti-oxidant strategies in Parkinson's disease.
The advance of Parkinson's disease has been suspected to be an outcome of oxidative stresses related to the metabolism of dopamine. Several recent studies have tested whether deprenyl (selegiline) or alpha-tocopherol (vitamin E) might attenuate the progression of Parkinson's disease. Although preliminary results of an 800-patient controlled clinical trial (DATATOP) suggested in 1989 that neuroprotection might be achieved with deprenyl, more recent analysis has questioned this conclusion. The apparent protective effect of deprenyl is lost after 1 year of treatment, and the drug's symptomatic antiparkinsonian effects confound an understanding of actions on the underlying disease. In the DATATOP trial, no neuroprotection was achieved with alpha-tocopherol. Methods developed in the deprenyl trials and newly discovered CSF markers of Parkinson's disease may be useful tools for future investigations of neuroprotective strategies against Parkinson's disease.
Wayne State University, School of Medicine, Detroit, Mich.
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LeWitt
D000975:Antioxidants / Q000008:administration & dosage*; D003342:Corpus Striatum / Q000187:drug effects / Q000503:physiopathology; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D008995:Monoamine Oxidase / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology / Q000517:prevention & control*; D017382:Reactive Oxygen Species / Q000378:metabolism; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D012642:Selegiline / Q000008:administration & dosage; D013378:Substantia Nigra / Q000187:drug effects / Q000503:physiopathology; D014810:Vitamin E / Q000008:administration & dosage
D000975:Antioxidants; D017382:Reactive Oxygen Species; D011954:Receptors, Dopamine; D014810:Vitamin E; D012642:Selegiline; D008995:Monoamine Oxidase; D004298:Dopamine