Perspectives on MAO-B in Aging and Neurological Disease:
Where Do We Go From Here?

Kumar MJ, Andersen JK.
Buck Institute for Age Research,
Novato, CA 94945.
Mol Neurobiol. 2004 Aug;30(1):77-90


The catecholamine-oxidizing enzyme monoamine oxidase-B (MAO-B) has been hypothesized to be an important determining factor in the etiology of both normal aging and age-related neurological disorders such as Parkinson's disease (PD). Catalysis of substrate by the enzyme produces H2O2 which is a primary originator of oxidative stress which in turn can lead to cellular damage. MAO-B increases with age as does predisposition towards PD which has also been linked to increased oxidative stress. Inhibition of MAO-B, along with supplementation of lost dopamine via L-DOPA, is one of the major antiparkinsonian therapies currently in use. In this review, we address several factors contributing to a possible role for MAO-B in normal brain aging and neurological disease and also discuss the use of MAO-B inhibitors as drug therapy for these conditions.

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Rasagiline/ anti-apoptotic bcl-2 gene family
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Rasagiline v selegiline: neuronal survival effects
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