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Migraine: gene mutations and functional consequences.

Arn M J M van den Maagdenberg1, Joost Haan, Gisela M Terwindt

  • 1Department of Human Genetics, Leiden, The Netherlands.

Current Opinion in Neurology
|May 15, 2007
PubMed
Summary
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Genetic studies reveal ion transport defects in familial hemiplegic migraine (FHM). While FHM genes are identified, common migraine genetics remain elusive, hindering understanding of this complex neurological disorder.

Area of Science:

  • Neurology
  • Genetics
  • Molecular Biology

Background:

  • Familial hemiplegic migraine (FHM) is a subtype of migraine with aura.
  • Genetic and functional studies have implicated ion transport dysfunction in FHM pathophysiology.
  • Identifying genes for common, multifactorial migraine presents significant challenges.

Purpose of the Study:

  • To review recent genetic and functional findings in familial hemiplegic migraine.
  • To discuss the role of ion transport and cortical spreading depression in migraine.
  • To highlight the difficulties in gene discovery for common migraine.

Main Methods:

  • Analysis of genetic mutations in FHM genes (FHM1, FHM2, FHM3).
  • Functional studies of identified mutations.

Related Experiment Videos

  • Exploration of novel genetic approaches for common migraine, including chromosomal loci identification.

    • Main Results:

    • Several new mutations in FHM1, FHM2, and FHM3 genes have been identified.
    • Functional consequences suggest a role for cortical spreading depression in migraine.
    • New genetic approaches for common migraine have been tested, but no specific gene variants have been found.

    Conclusions:

    • Disturbed ion transport is a major factor in familial hemiplegic migraine.
    • Cellular and mouse models indicate increased potassium and glutamate contribute to FHM pathophysiology.
    • Despite advances in FHM research, the genetic basis of common migraine remains undiscovered.