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• W25768368 abstract "Deprenyl, a monoamine oxidase inhibitor used in the treatment of Parkinson's disease, along with its primary metabolite desmethyldeprenyl (DES) have been shown to reduce neuronal apoptosis by a mechanism that requires gene transcription and involves the maintenance of mitochondrial membrane potential. This review article explores the mechanisms by which DES maintains mitochondrial membrane potential. Mediated by GAPDH binding, DES increases mitochondrial BCL-2 and BCL-xL levels and decreases BAX levels thereby preventing the permeability transition pore (PTP) form opening and preventing apoptotic degradation. The favorable effects of deprenyl on neuronal apoptosis suggests the therapeutic potential of designing compounds with the capacity to alter the configurations of pro-apoptosis or anti-apoptotic proteins." @default.
• W25768368 created "2016-06-24" @default.
• W25768368 creator A5051864168 @default.
• W25768368 date "1999-01-01" @default.
• W25768368 modified "2023-09-23" @default.
• W25768368 title "Apoptotic Mechanisms in Neurodegeneration: Possible Relevance to Glaucoma" @default.
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• W25768368 doi "https://doi.org/10.1177/112067219900901s10" @default.
• W25768368 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10230602" @default.
• W25768368 hasPublicationYear "1999" @default.
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