Abstract

The deprenyl and tocopherol antioxidative treatment (DATATOP) study has shown that selegiline (deprenyl), with or without tocopherol, reduces physical and psychological deficits in patients with Parkinson's disease within one month of treatment and reduces the probability of reaching a primary endpoint, the decision to treat with levodopa. This paper critically re-evaluates the inference that selegiline has a neuroprotective effect and thus delays progression of Parkinson's disease. Analysis is based on a simple model which assumes that clinically measured impairment is proportional to degree of cellular dysfunction in Parkinson's disease. The analysis suggests that the reduced probability of reaching an endpoint was due to a direct treatment effect rather than to neuroprotection.