Editorials

Selegiline in Parkinson's disease

BMJ 1995; 311 doi: http://dx.doi.org/10.1136/bmj.311.7020.1583 (Published 16 December 1995) Cite this as: BMJ 1995;311:1583
  1. Donald B Calne
  1. Director Neurodegenerative Disorders Centre, Faculty of Medicine, Vancouver Hospital and Health Sciences Centre, Vancouver, BC, Canada V6T 2B5

    >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 “neuroprotection” in chronic neurodegenerative disease. The largest of these trials was DATATOP (deprenyl and tocopherol antioxidant therapy for parkinsonism),3 …

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