Advance in genetics of migraine

Boer, Irene de; Maagdenberg, Arn M. J. M. van den; Terwindt, Gisela M.

doi:10.1097/wco.0000000000000687

Cited by 71 publications

(59 citation statements)

References 40 publications

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“…Moreover, migraine is a polygenic disease with the contribution of multiple genetic variants, each of them having a relatively small effect. It is believed that migraine development is a result of the complex interaction of numerous gene variants and epigenetic mechanisms with both environmental and lifestyle factors [ 24 , 26 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

Analysis of Genetic Variants in SCN1A, SCN2A, KCNK18, TRPA1 and STX1A as a Possible Marker of Migraine

Kowalska

Prendecki

Kapelusiak-Pielok

et al. 2020

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Background: Migraine is a polygenetic disease, considered as a channelopathy. The dysregulation of ion functioning due to genetic changes may activate the trigeminovascular system and induce migraine attack both migraine with aura (MA) and without aura (MO). Objectives: The aim of the study was to analyze the following variants of genes encoding ion channels and associated protein: c.3199G>A SCN1A, c.56G>A SCN2A, c.28A>G and c.328T>C KCNK18, c.3053A>G TRPA1, c.31-1811C>T STX1A in migraine patients. Patients and Methods: The study included 170 migraine patients and 173 controls. HRMA and Sanger sequencing were used for genotyping. Meta-analysis was performed for c.28A>G, c.328T>C KCNK18, and c.31-1811C>T STX1A. Patients and Methods: The study included 170 migraine patients and 173 controls. HRMA and Sanger sequencing were used for genotyping. Meta-analysis was performed for c.28A>G, c.328T>C KCNK18, and c.31-1811C>T STX1A. Results: AA genotype of c.56G>A SCN2A was found only in migraine patients. Patients with c.328T>C KCNK18 mutation had an increased risk of developing migraine before the age of 18. Moreover, individuals with AA/TC haplotype of KCNK18 had higher attack frequency than those with AA/TT (p<0.05). T allele of c.31-1811C>T STX1A was more frequent in MA patients than MO (p<0.05). The c.3053A>G TRPA1 polymorphism was more common in patients with migraine onset before the age of 15 (p<0.05), while c.31-1811C>T STX1A and c.3199G>A SCN1A before the age of 10 (p<0.01). Meta-analysis showed a significant association of c.31-1811C>T STX1A polymorphism with migraine overall (OR=1.22, p=0.0086), MA, and MO. No association was found for c.28A>G KCNK18, c.328T>C KCNK18, and migraine overall. Conclusions: Changes in genes encoding ion channels or proteins regulating their functioning may increase the risk of migraines and correlate with clinical features of disease, e.g. age of onset and attack frequency.

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Section: Discussionmentioning

confidence: 99%

Analysis of Genetic Variants in SCN1A, SCN2A, KCNK18, TRPA1 and STX1A as a Possible Marker of Migraine

Kowalska

Prendecki

Kapelusiak-Pielok

et al. 2020

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“…Most cases of VM are considered sporadic, but familial aggregation of VM with autosomal-dominant inheritance has been described in several families, supporting a genetic background for the condition (3,4). Genome-wide association studies (GWASs) have identified numerous single-nucleotide polymorphisms (SNPs) associated with a genetic predisposition for migraine with or without aura (5,6). Familial hemiplegic migraine (FHM), which is a subtype of migraine with aura, is caused by mutations in CACNA1A, ATP1A2, and SCN1A (7).…”

Section: Introductionmentioning

confidence: 99%

TRPM7 as a Candidate Gene for Vestibular Migraine

Shin

Cho

et al. 2020

Front. Neurol.

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Objectives: Vestibular migraine (VM) is a common vestibular disorder, and familial aggregation of VM with autosomal-dominant inheritance has been described, which supports a genetic background. This study aimed to describe the clinical phenotype of a family with VM, and identify a candidate gene for VM. Methods: We recruited six individuals (four affected and two unaffected) from three consecutive generations of a Korean family with VM, and performed whole-exome sequencing to search for candidate genes. Results: All affected individuals presented with recurrent vertigo, headache, and nausea/vomiting that fulfilled the diagnostic criteria of VM. Two individuals also experienced transient hemiparesis or dysarthria during the episodes. The symptoms were triggered by physical or emotional stress. Interictal examinations showed uni-or bi-directional horizontal gaze-evoked nystagmus in three of the individuals. They had no causative mutations in genes causing familial hemiplegic migraine or episodic ataxia. Through whole-exome sequencing from three affected individuals, we identified a nonsense mutation c.3526C>T in TRPM7 that encodes a cation channel selective to Ca 2+ and Mg 2+. Conclusions: Alterations in intracellular Ca 2+ and Mg 2+ homeostasis by TRPM7 mutation may contribute to the development of the VM phenotype. Our result suggest that TRPM7 is a novel candidate gene for VM.

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“…Migraine is caused by mutations in the CACNA1A (Calcium voltage-gated channel subunit alpha1 A), ATP1A2 (ATPase Na+/K+ transporting subunit alpha 2) and SCN1A (Sodium voltage-gated channel alpha subunit 1) genes. 6 The CACNA1A gene sends signals for making one part (the alpha-1 subunit) of a calcium channel called CaV2.1. This subunit forms the pore through which calcium ions can flow.…”

Section: Introductionmentioning

confidence: 99%

Biocomputational Analysis Establishes Genetic Association of Rheumatoid Arthritis (RA) and Migraine

Roy¹,

Mazumder

2020

Preprint

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An autoimmune disease and a neurological disease do not tie up together but if statistics say that 61% of people are affected by Rheumatoid Arthritis (an autoimmune disease) and Migraine (a neurological disease) at the same time it is really a point to be noted. The previous studies show that Rheumatoid Arthritis (RA) and Migraine are related anatomically but our goal was to dig out any other similarities except it. Therefore, we studied their genes and hoped to get something fascinating. We assessed the genes from the literature study and Genetic Home Reference (https://ghr.nlm.nih.gov/). After that, the genetic sequences of these genes were extracted from NCBI (National Center for Biotechnology Information, http://ncbi.nlm.nih.gov) and by applying multiple sequence alignment, we created a phylogenetic tree by Mega (Molecular Evolutionary Genetics Analysis). Surprisingly, we found 10 pairs of genes with similar genetic structures and common ancestry. Therefore, we can say these 10 pairs of genes are related to each other closely, which is why Migraine and Rheumatoid Arthritis (RA) are found together in a person. At the last part of this study, we used protein expression for the evaluation of the result. Here our bioinformatics approach may help to strengthen the connectedness of these two diverse diseases.

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Advance in genetics of migraine

Cited by 71 publications

References 40 publications

Analysis of Genetic Variants in SCN1A, SCN2A, KCNK18, TRPA1 and STX1A as a Possible Marker of Migraine

Analysis of Genetic Variants in SCN1A, SCN2A, KCNK18, TRPA1 and STX1A as a Possible Marker of Migraine

TRPM7 as a Candidate Gene for Vestibular Migraine

Biocomputational Analysis Establishes Genetic Association of Rheumatoid Arthritis (RA) and Migraine

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