Molecular Neurobiology

, Volume 30, Issue 1, pp 77–89

Perspectives on MAO-B in aging and neurological disease

Where do we go from here?

Authors

  • M. Jyothi Kumar
    • Buck Institute for Age Research
  • Julie K. Andersen
    • Buck Institute for Age Research
Article

DOI: 10.1385/MN:30:1:077

Cite this article as:
Kumar, M.J. & Andersen, J.K. Mol Neurobiol (2004) 30: 77. doi:10.1385/MN:30:1:077

Abstract

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.

Index Entries

Monoamine oxidase BParkinson’s diseaseagingfree radicalsdeprenylgenetic polymorphismsmitochondrial dysfunction

Copyright information

© Humana Press Inc 2004