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Apoptotic mechanisms in neurodegeneration: possible relevance to glaucoma.

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.

PMID: 10230602, UI: 99247217
Tatton WG
Eur J Ophthalmol 1999 Jan-Mar;9 Suppl 1:S22-9
Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA.
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http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10230602&form=6&db=m
&Dopt=b

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janet paterson   52 now 41 dx 37 onset  [log in to unmask]
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