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Brian Collins wrote: > .... I have been taking Vitamin E for the past 6 or 8 years ... > During that 6 or 8 years, my PD has not deviated one bit in its > downward trend... According to a recent article, the current thinking seems to be that "oxident stress" is one component of several involved in the disease mechanism: "Whatever initiates PD, be it a genetic abberation, an environmental toxin, or a combination of both.... It now appears that a number of interacting themes form a cascade of procesess culminating in nigral cell death. These include oxident stress, mitochondrial dysfunction, excitotoxicity with excess nitric oxide formation, and glial and inflammatory processes. It is now held that the final culmination of these events is the induction of apoptosis in nigral dopaminergic neurons.... "....Clinical trials to date have largely focused on vitamin E and deprenyl. Vtamin E in oral doses of 2,000 IU was found to have no effect. Deprenyl slowed the emergence of disability and the progression of signs and symptoms....Further clinical trials are warranted to test other antioxidant agents...." (Marsden CD and Olanow, CW, "The causes of Parkinson's disease are being unraveled and rational neuroprotective therapy is close to reality", Annals of Neurology 1998(Suppl 1):S189-S196.) What I've read and what I once heard Dr. Thomas Chase of the NIH say is that Vitamin E does not cross the blood/brain barrier. There are other antioxidents that do. Coenzyme Q10, which is both a free radical scavenger and a component of the cell energy producing process, has been shown to be neuroprotective in animal models of Huntington's disease and ALS when taken orally. (Matthews MT et al, "Coenzyme Q10 administration increases brain mitochondial concentrations and exerts neuroprotective effects", Proceedings of the National Academy of Science, Vol. 95, Issue 15, PP 8892-8897, July 21, 1998.) Clinical trials of coenzyme Q10 are now under way, and it will be interesting what they show. Phil Tompkins Hoboken NJ age 61/dx 1990