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 α-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 DAT ATOP trial, no neuroprotection was achieved with a-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.

Keywords:
Parkinson’s disease, Deprenyl, Monoamine oxidase, Controlled clinical trial, Anti-oxidant therapy
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© 1993 S. Karger AG, Basel
1993
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