Neurogenetics

, Volume 6, Issue 2, pp 67–72

A genome-wide scan provides evidence for loci influencing a severe heritable form of common migraine

Authors

  • R. A. Lea
    • Genomics Research Centre, School of Health ScienceGriffith University
    • Institute of Environmental Science and Research
  • D. R. Nyholt
    • Genetic Epidemiology LaboratoryQueensland Institute of Medical Research
  • R. P. Curtain
    • Genomics Research Centre, School of Health ScienceGriffith University
  • M. Ovcaric
    • Genomics Research Centre, School of Health ScienceGriffith University
  • R. Sciascia
    • Genomics Research Centre, School of Health ScienceGriffith University
  • C. Bellis
    • Genomics Research Centre, School of Health ScienceGriffith University
  • J. MacMillan
    • Queensland Clinical Genetics Service, Royal Children’s Hospital
  • S. Quinlan
    • Genomics Research Centre, School of Health ScienceGriffith University
  • R. A. Gibson
    • GlaxoSmithKline Medicines Research Centre
  • L. C. McCarthy
    • GlaxoSmithKline Medicines Research Centre
  • J. H. Riley
    • GlaxoSmithKline Medicines Research Centre
  • Y. J. Smithies
    • GlaxoSmithKline
  • S. Kinrade
    • GlaxoSmithKline Pharmaceuticals Division
    • Genomics Research Centre, School of Health ScienceGriffith University
Original Article

DOI: 10.1007/s10048-005-0215-6

Cite this article as:
Lea, R.A., Nyholt, D.R., Curtain, R.P. et al. Neurogenetics (2005) 6: 67. doi:10.1007/s10048-005-0215-6

Abstract

Migraine is a prevalent neurovascular disease with a significant genetic component. Linkage studies have so far identified migraine susceptibility loci on chromosomes 1, 4, 6, 11, 14, 19 and X. We performed a genome-wide scan of 92 Australian pedigrees phenotyped for migraine with and without aura and for a more heritable form of “severe” migraine. Multipoint non-parametric linkage analysis revealed suggestive linkage on chromosome 18p11 for the severe migraine phenotype (LOD*=2.32, P=0.0006) and chromosome 3q (LOD*=2.28, P=0.0006). Excess allele sharing was also observed at multiple different chromosomal regions, some of which overlap with, or are directly adjacent to, previously implicated migraine susceptibility regions. We have provided evidence for two loci involved in severe migraine susceptibility and conclude that dissection of the “migraine” phenotype may be helpful for identifying susceptibility genes that influence the more heritable clinical (symptom) profiles in affected pedigrees. Also, we concluded that the genetic aetiology of the common (International Headache Society) forms of the disease is probably comprised of a number of low to moderate effect susceptibility genes, perhaps acting synergistically, and this effect is not easily detected by traditional single-locus linkage analyses of large samples of affected pedigrees.

Keywords

MigraineSusceptibilityGenome scanLoci

Copyright information

© Springer-Verlag 2005