BMJ 1995;311:1583-1584 (16 December)

Editorials

Selegiline in Parkinson's disease

No neuroprotective effect: increased mortality

In medicine, as in all other human activities, fashions come and go. In the field of Parkinson's disease, there has been an explosion of research on the possibility that nerve cells in the substantia nigra are dying because of excessive production of toxic free radicals. The "oxidative stress" hypothesis envisions dopamine undergoing oxidative metabolism to produce an excess of free radicals that gradually kill the dopaminergic neurons, which bear the brunt of the pathology of Parkinson's disease.1 But there is no compelling evidence for this view2; at best damage by free radicals might represent the final common pathway to cell death, just as cessation of the heart-beat is an inevitable feature of corporeal death.

In its heyday, the free radical hypothesis fuelled enormous therapeutic trials for Parkinson's disease, based on the premise that if we could reduce formation of free radicals this would confer . . . [Full text of this article]


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