摘要：

Several members of the neurotrophin, mitogen, and cytokine/neurokine families have the capacity to reduce or slow neuronal apoptosis. Each of these neurotrophic factors act on specific receptors, which activate a number of cellular processes, some of which lead to a reduction in neuronal death. Deprenyl was synthesized as a psychoenergizer that combined ()-metham–phetamine with a pargene chain and was subsequently found to selectively inhibit the B form of monoamine oxidase (MAO-B). Levodopa and ()-deprenyl were used in combination to treat Parkinson's disease in the hope that levodopa would be converted to dopamine by nigrostriatal neurones, and ()-deprenyl would cause an acute decrease in dopamine metabolism, thereby increasing dopamine availability in the striatum. The celebrated finding that MAO-B inhibition protected nigrostriatal neurones from damage caused by the toxin MPTP, presumably by blocking the conversion of 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) to 1-methyl-4-phenylpyridinum (MPP + ) in astroglia, reinforced the view that ()-deprenyl could have clinical utility as an MAO-B inhibition-dependent neuroprotectant. The results indicate that three of the four MAO-independent actions of ()-deprenyl result from selective alterations in gene expression induced by ()-desmethyldeprenyl.

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