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

Mol Neurobiol. 2004 Aug;30(1):77-89. 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.

Publication types

  • Review

MeSH terms

  • Aging / drug effects
  • Aging / genetics
  • Aging / physiology*
  • Animals
  • Brain / drug effects
  • Brain / enzymology
  • Humans
  • Monoamine Oxidase / genetics
  • Monoamine Oxidase / physiology*
  • Monoamine Oxidase Inhibitors / pharmacology
  • Monoamine Oxidase Inhibitors / therapeutic use
  • Nervous System Diseases / drug therapy
  • Nervous System Diseases / enzymology*
  • Nervous System Diseases / genetics

Substances

  • Monoamine Oxidase Inhibitors
  • Monoamine Oxidase