Monoamine oxidases A and B gene polymorphisms in migraine patients

J Neurol Sci. 2005 Feb 15;228(2):149-53. doi: 10.1016/j.jns.2004.11.045. Epub 2004 Dec 24.

Abstract

Abnormal cortical activity and brainstem functioning are considered the possible etiopathogenetic factors of migraine. Monoamine oxidase A and B (MAO-A and -B) regulate the levels of monoamine neurotransmitters, so changes in their activity could participate in migraine pathogenesis. We have investigated the possible association of MAO-A and -B alleles and haplotypes with two common types of migraine, i.e. migraine without aura (MO) and migraine with aura (MA), on the sample of 110 migraineours (80 MO and 30 MA) and 150 controls. MAO-A promoter and MAO-B intron 13 polymorphisms were genotyped by the PCR-based methods. In addition, we have reevaluated the reported association between MAO-B intron 13 polymorphism and platelet MAO-B activity. The platelet MAO-B activity was determined fluorimetrically using kynuramine as a substrate. We have found a tendency toward association of the shorter variant of MAO-A gene promoter with migraine without aura in male subjects. Regarding investigated MAO-B polymorphism, no association with migraine or with platelet MAO-B activity was found. The suggestive association of the variant in MAO-A gene with migraine is considered worthy of independent replication. On the other hand, further studies on MAO-B polymorphism in migraine do not seem promising.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Biogenic Monoamines / metabolism*
  • Blood Platelets / enzymology
  • Brain / enzymology*
  • Brain / pathology
  • Brain / physiopathology
  • DNA Mutational Analysis
  • Female
  • Gene Frequency / genetics
  • Genetic Markers / genetics
  • Genetic Testing
  • Genotype
  • Haplotypes / genetics
  • Humans
  • Introns / genetics
  • Male
  • Middle Aged
  • Migraine Disorders / blood
  • Migraine Disorders / enzymology*
  • Migraine Disorders / genetics*
  • Monoamine Oxidase / genetics*
  • Polymorphism, Genetic / genetics*
  • Promoter Regions, Genetic / genetics
  • Sex Factors

Substances

  • Biogenic Monoamines
  • Genetic Markers
  • Monoamine Oxidase