Abstract

Abstract Genetics of migraine has recently undergone a major shift, moving in the space of a few years from having only a few known genes for rare Mendelian forms to 47 known common variant loci affecting the susceptibility of the common forms of migraine. This has largely been achieved by rapidly increasing sample sizes for genomewide association studies (GWAS), soon to be followed by the first wave of large-scale exome-sequencing studies. The large number of detected loci, chief among them TRPM8, PRDM16, and LRP1, have enabled a number of in silico analyses, which have shed light on the functional and tissue-level aspects of the common risk variants for migraine, including evidence for involvement of both vascular and neuronal mechanisms. Polygenic risk scores and other measures of genetic variance based on GWAS information are further opening the door to dissecting pharmacogenetics, functional etiology, and comorbidity. Heritability-based analyses are demonstrating strong links between migraine and other neuropsychiatric disorders and brain phenotypes, highlighting genetic links between migraine and major depressive disorder and attention-deficit hyperactivity disorder, among others. These recent successes in migraine genetics are starting to be mature enough to provide robust evidence of specific quantifiable genetic factors in common migraine.
Original languageEnglish
Title of host publicationHandbook of Clinical Neurology : Neurogenetics, Part II
EditorsDaniel H. Geschwind, Henry L. Paulson, Christine Klein
Number of pages11
Volume148
PublisherElsevier
Publication date2018
Edition1st ed.
Pages493-503
ISBN (Print)978-0-444-64076-5
ISBN (Electronic)978-0-444-64077-2
DOIs
Publication statusPublished - 2018
MoE publication typeA3 Book chapter

Fields of Science

  • migraine
  • genetics
  • neurology
  • GWAS
  • familial hemiplegic migraine
  • heritability analysis
  • 3111 Biomedicine
  • 3112 Neurosciences
  • 3124 Neurology and psychiatry

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