4.6 Review

Perspectives on MAO-B in aging and neurological disease - Where do we go from here?

Journal

MOLECULAR NEUROBIOLOGY
Volume 30, Issue 1, Pages 77-89

Publisher

SPRINGER
DOI: 10.1385/MN:30:1:077

Keywords

monoamine oxiclase B; Parkinson's disease; aging; free radicals; deprenyl; genetic polymorphisms; mitochondrial dysfunction

Categories

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available