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T. S. Elizan, MD; D. A. Moros, MD; M. D. Yahr, MD
Department of Neurology Mount Sinai Medical Center, Box 1137 One Gustave L. Levy Pl New York, NY 10029

Arch Neurol. 1991;48(10):1009-1010.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.

—We thank Hauser and Olanow for their comments and appreciate the various therapeutic strategies that they propose and which have been detailed in a previous publication.¹ Since their suggestions rely heavily on the results of the DATATOP study,^2,3 a comment on its design and interpretation is in order. DATATOP was designed as a clinical trial to test the intriguing hypothesis (originally suggested by Birkmayer et al⁴ in 1985) that long-term monoamine oxidase type B (MAO-B) inhibition with the drug, selegiline (L-deprenyl), will provide a "protective" effect on nigral degeneration and slow the progression of Parkinson's disease (PD). To date, this hypothesis remains unproven. The DATATOP results demonstrate an effect on the clinical status of treated patients compared with untreated control subjects receiving no active symptomatic treatment of any kind. The delay in the needfor levodopa (the authors' end point) in the selegiline-treated patients compared . . . [Full Text PDF of this Article]

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