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Mol Genet Genomics. 2017 Aug;292(4):729-739. doi: 10.1007/s00438-017-1317-1. Epub 2017 Apr 7.

Ion channelopathies and migraine pathogenesis.

Author information

1
Genomics Research Centre, Institute for Biomedical Health and Innovation, Queensland University of Technology, Brisbane, QLD, 4059, Australia.
2
Genomics Research Centre, Institute for Biomedical Health and Innovation, Queensland University of Technology, Brisbane, QLD, 4059, Australia. lyn.griffiths@qut.edu.au.

Abstract

Migraine is a common neurological disorder that affects approximately 12-20% of the general adult population. Migraine pathogenesis is complex and not wholly understood. Molecular genetic investigations, imaging and biochemical studies, have unveiled a number of interconnected neurological pathways which seem to have a cause and effect component integral to its cause. Much weight of migraine attack initiation can be placed on the initial trigger and the pathways involved in its neuronal counter reaction. Ion channels play a large role in the generation, portrayal and mitigation of the brains response to external triggers. Several genetic studies have identified and implicated a number of ion channelopathy genes which may contribute to this generalised process. This review will focus on the genetics of migraine with particular emphasis placed on the potentially important role genes HEPH (responsible for iron transport and homeostasis) and KCNK18 (important for the transport and homeostasis of potassium) play in migraine cause.

KEYWORDS:

HEPH; Hephaestin; Ion channelopathies; KCNK18; Migraine; TRESK

PMID:
28389699
DOI:
10.1007/s00438-017-1317-1
[Indexed for MEDLINE]

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