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. 2011 Mar 21;3(3):17.
doi: 10.1186/gm231.

Towards an understanding of genetic predisposition to migraine

Verneri Anttila  1 , Maija Wessman, Mikko Kallela, Aarno Palotie
Affiliations

Towards an understanding of genetic predisposition to migraine

Verneri Anttila et al. Genome Med. .

Abstract

Plausible genome-wide associations for episodic neurological diseases (such as migraine, epilepsy and ataxias) have been slow to emerge. The first such association was reported in a recent genome-wide association study of migraine, with quantitative expression analysis linking the variant to a nearby regulatory gene, MTDH/AEG-1. This putative mechanism, regulating the expression of the primary glutamate transporter in the brain, EAAT2/GLT-1, has interesting implications bridging the gap between Mendelian and common forms in this key group of disorders.

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Figures

Figure 1
Figure 1
Localization and effect of a variant identified in the recent genome-wide association study of migraine in synaptic transmission, together with the previously known mutations in familial hemiplegic migraine (FHM: genes are FHM1, CACNA1A; FHM2, ATP1A2; FHM3, SCN1A). The asterisk indicates the excitatory amino acid transporter 2 (EAAT2/GLT-1) recently linked to migraine. Glu, glutamate; FHM1-3, products of genes reported for familial hemiplegic migraine; mGluR, metabolic glutamate receptor. Black dots indicate the accumulation of the neurotransmitter glutamate in the synaptic cleft.
See this image and copyright information in PMC

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