Apoptotic Mechanisms in Neurodegeneration: Possible Relevance to Glaucoma
| Autor: | Tatton Wg |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
0301 basic medicine
Monoamine Oxidase Inhibitors medicine.drug_class bcl-X Protein Apoptosis Bcl-xL Neuroprotection Membrane Potentials 03 medical and health sciences 0302 clinical medicine Proto-Oncogene Proteins Selegiline medicine Animals Humans Glyceraldehyde 3-phosphate dehydrogenase bcl-2-Associated X Protein Membrane potential Monoamine oxidase inhibitor biology Mechanism (biology) Chemistry Neurodegeneration Glyceraldehyde-3-Phosphate Dehydrogenases Glaucoma Optic Nerve General Medicine medicine.disease Mitochondria Cell biology Ophthalmology 030104 developmental biology Proto-Oncogene Proteins c-bcl-2 Nerve Degeneration biology.protein 030217 neurology & neurosurgery |
| Zdroj: | European Journal of Ophthalmology. 9:S22-S29 |
| ISSN: | 1724-6016 1120-6721 |
| DOI: | 10.1177/112067219900901s10 |
| Popis: | 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) from 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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