title: Perspectives on MAO-B in aging and neurological disease: where do we go from here?
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.
authors.affiliation: Buck Institute for Age Research, Novato, CA 94945, USA.
authors.forename: M Jyothi
authors.initials: MJ
authors.lastname: Kumar
authors.forename: Julie K
authors.initials: JK
authors.lastname: Andersen
mesh_terms: D000375:Aging / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000201:enzymology; D006801:Humans; D008995:Monoamine Oxidase / Q000235:genetics / Q000502:physiology*; D008996:Monoamine Oxidase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D009422:Nervous System Diseases / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics
chemical_list: D008996:Monoamine Oxidase Inhibitors; D008995:Monoamine Oxidase