Abstract
Migraine is a common neurovascular condition. This disorder has a complex genetic background. Several single-nucleotide polymorphisms (SNPs) or mutations within genes regulating glutamatergic neurotransmission, cortical excitability, ion channels, and solute carriers have been associated with polygenic and monogenic forms of migraine. SNPs within ACE, DBH, TRPM8, COMT, GABRQ, CALCA, TRPV1, and other genes have been reported to affect the risk of migraine or the associated clinical parameters. The distribution of some HLA alleles within the HLA-DRB1, HLA-DR2, HLA-B, and HLA-C regions have also been found to differ between migraineurs and healthy subjects. In addition, certain mitochondrial DNA changes and polymorphisms in this region have been shown to increase the risk of migraine. A few functional studies have investigated the molecular mechanisms contributing to these genetic factors in the development of migraine. Here we review studies evaluating the role of genetic polymorphisms and mRNA/miRNA dysregulation in migraine.
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