Summary.
Deprenyl and other propargylamines are clinically beneficial in Parkinson's disease (PD). The benefits were thought to depend on monoamine oxidase B (MAO-B) inhibition. A large body of research has now shown that the propargylamines increase neuronal survival independently of MAO-B inhibition by interfering with apoptosis signaling pathways. The propargylamines bind to glyceraldehyde-3-phosphate dehydrogenase (GAPDH). The GAPDH binding is associated with decreased synthesis of pro-apoptotic proteins like BAX, c-JUN and GAPDH but increased synthesis of anti-apoptotic proteins like BCL-2, Cu-Zn superoxide dismutase and heat shock protein 70. Anti-apoptotic propargylamines that do not inhibit MAO-B are now in PD clinical trial.
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Received December 9, 2002; accepted December 12, 2002
Authors' address: Dr. W. G. Tatton, Mount Sinai School of Medicine, Department of Neurology, One Gustave L. Levy Place, Annenburg 1470, Box 1137, New York, NY 10029-6574, U.S.A., e-mail: william.tatton@mssm.edu
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Tatton, W., Chalmers-Redman, R. & Tatton, N. Neuroprotection by deprenyl and other propargylamines: glyceraldehyde-3-phosphate dehydrogenase rather than monoamine oxidase B. J Neural Transm 110, 509–515 (2003). https://doi.org/10.1007/s00702-002-0827-z
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DOI: https://doi.org/10.1007/s00702-002-0827-z