Lack of association between oxidative stress-related gene polymorphisms and chronic migraine in an Italian population

Abstract

Migraine patients present increased risks of vascular diseases such as high blood pressure, insulin resistance, metabolic syndrome, stroke and coronary heart disease. Oxidative stress (OS) is increasingly being studied in relation to the pathophysiology of migraine, stimulated by the described association with the most frequent migraine comorbidities. Because many of the gene-encoded players of the OS balance are characterized by functional polymorphisms, it is supposed that the individual genomic profile could affect susceptibility to OS and to related pathophysiological conditions. This study aimed to characterize a panel of 10 polymorphisms in 8 OS-related genes in a chronic migraine (CM) population and healthy controls, to recognize a genetic risk in the process of migraine chronification. The sample consisted of 45 healthy women and 96 women diagnosed with CM. No deviations from the Hardy-Weinberg equilibrium were detected, or in the overall population, or in the CM group or in the control group.

From transformation to chronification of migraine: pathophysiological and clinical aspects

“…Oxidative stress is a subject increasing in popularity regarding its relation to the pathophysiology of migraine. However, a study that investigated 10 polymorphisms in 8 oxidative stress-related genes in a small population of CM patients did not detect a relationship with CM [51]. However, as migraine is considered a complex disease with multifactorial inheritance, Genome-Wide Association Study (GWAS) seems a more appropriate approach to study migraine genetic background.…”

Chronic Migraine in Adolescence

“…However, so far studies have not shown association between gene polymorphisms associated with oxidative stress and the occurrence of CM. On the other hand, repetitive painful stimuli on the trigeminal nerve cause activation of the pain modulating descending system in several portions, including the periaqueductal gray matter, showing that during migraine attacks, the neurons of this region show increased activity, which may lead to oxidative stress and finally dysfunction of nociceptive modulation by such system [33,[41][42][43].…”

A systematic review and critical appraisal of gene polymorphism association studies in medication-overuse headache

“…The search strategy on PubMed and Web of Knowledge identified a total of 128 studies, of which 16 were duplicates. After the removal of 95 hits not fulfilling the inclusion criteria, 17 studies were finally included in the qualitative review of gene association studies focusing on MOH (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38). The main characteristics of the identified studies are summarized in Table 1 between 2006 and 2015 by five research groups, four of which were located in Italy -including our group -and one in Japan, with sample sizes of MOH patients ranging from 22 to 227.…”

“…The main characteristics of the identified studies are summarized in Table 1 between 2006 and 2015 by five research groups, four of which were located in Italy -including our group -and one in Japan, with sample sizes of MOH patients ranging from 22 to 227. Twelve studies had a case-control design (22,(25)(26)(27)(28)(29)(31)(32)(33)(34)36,37), while the remaining five were case-only studies (23,24,30,35,38). Thirteen studies were conducted on MOH patients with Caucasian ancestry (22)(23)(24)(25)(26)(27)29,30,(34)(35)(36)(37)(38), while four studies recruited MOH patients with Asian ethnicity (28,(31)(32)(33).…”

“…Twelve case-control studies investigated the role of common genetic polymorphisms as risk factors for MOH susceptibility (22,(25)(26)(27)(28)(29)(31)(32)(33)(34)36,37). Overall, 50 polymorphisms were analysed in 33 genes related to serotoninergic transmission (SLC6A4, 5HT1A, 5HT2A, 5HT1B, GNB3, 5HT6, TPH2), dopaminergic transmission (SLC6A3, COMT, DBH, DRD2 and DRD4), drug dependence (ACE, OPRM1, BDNF, EEAT2), metabolic pathways (CYP1A2, MAOA, MTHFR), oxidative stress (eNOS, nNOS, GTPCH, GSTP1, GSTM1, GSTT1, SOD, CAT, PON, CYBA), CGRP pathway (CALCA, RAMP1), and genes postulated to be relevant for migraine pathophysiology (ESR1, TNF-b).…”