Cytochrome P450 2D6 and glutathione S‐transferase M1 genotypes and migraine

Mattsson, Peter; Bjelfman, C; Lundberg, P. O.; Rane, Anders

doi:10.1046/j.1365-2362.2000.00633.x

Cited by 11 publications

(4 citation statements)

References 20 publications

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“…Negative studies evaluating candidate genes for association with migraine have included evaluation of interleukin-6 (Rainero et al 2003), DRD1, DRD3, and DRD5 , apolipoprotein E/APOE (Rainero et al 2002a), 5HT1B receptor (Maassen Van Den Brink et al 1998, inducible nitric oxide synthase/iNOS (Lea et al 2001b), cytochrome P450 2D6/CYP2D6 and glutathione S-transferase M1/GSTM1 (Mattsson et al 2000), 5-HT2A and 5-HT2B (Buchwalder et al 1996;Nyholt et al 1996;Burnet et al 1997), a nitric oxide synthase polymorphism (Nyholt et al 1996), and the DRD3 and DRD4 dopamine receptor subtypes Del Zompo et al 1998).…”

Section: Genome Scans For Familial Migrainementioning

confidence: 99%

Update on the genetics of migraine

Estevez

Gardner

2004

Human Genetics

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The field of migraine genetics has seen an explosion of information over the last year. In a recent breakthrough, missense mutations in a chromosome 1q23 gene, ATP1A2, encoding a Na+, K+-ATPase, have been identified in four distinct pedigrees with a rare form of familial hemiplegic migraine (FHM). ATP1A2 is expressed in the brain, like the voltage gated calcium channel gene, CACNA1A, previously identified as the first hemiplegic migraine gene (FHM1). The shared hemiplegic migraine phenotype of mutations in ATP1A2 and CACNA1A raises the possibility that they coordinately regulate ion homeostasis that determines susceptibility to the initiation of both migraine aura and the pain phase of migraine. For the more common and genetically complex forms of migraine, genome-wide screens have identified several new loci on 4q24, 6p12.2-21.1, 11q24, and 14q21.2-q22.3, suggesting additional migraine genes in these regions. In addition, a recent large case-control association study has linked single nucleotide polymorphisms in the insulin receptor/INSR gene with migraine. However, these polymorphisms do not result in detectable changes in receptor function. The continuing genetic identification of key proteins involved in migraine will refine our understanding of this common and sometimes debilitating disorder, which can strike during the most productive years of a person's life. Given the co-morbidity of migraine with depression and bipolar disorder, our knowledge of the causes of migraine may also contribute to our understanding of these disorders.

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Section: Genome Scans For Familial Migrainementioning

confidence: 99%

Update on the genetics of migraine

Estevez

Gardner

2004

Human Genetics

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“…On the other hand, there were no differences between MWA and TH. Mattsson et al [16]found no association between the M1 polymorphism and migraine in a Swedish population. However, migraine patients were not classified as MWA or MWOA.…”

Section: Discussionmentioning

confidence: 99%

“…There have been several investigations of their association with an increased risk factor for cancer [11, 12, 13, 14, 15]. However, there has only been one report regarding GST gene polymorphism and migraine [16]. We investigated the polymorphisms of GSTM1, T1 and P1 in the Japanese migraine sufferer.…”

Section: Introductionmentioning

confidence: 99%

Glutathione S-Transferase Polymorphisms: Susceptibility to Migraine without Aura

et al. 2003

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Migraine is considered to be a polygenic multifactorial disease with various environmental and genetic etiologies. We investigated glutathione S-transferase (GST) P1 Ile¹⁰⁵Val, T1 and M1 polymorphisms in 174 Japanese headache sufferers and 372 Japanese controls. The headache group consisted of 38 cases of migraine with aura, 95 migraine without aura (MWOA) and 41 tension-type headache sufferers. The M1 homozygous deletion genotype was significantly higher in MWOA (64%) compared with controls (46%; p < 0.01; odds ratio = 2.18, 95% confidence interval: 1.32–3.61, adjusted for age and gender). In a comparison of the current smokers, the M1 null frequencies in MWOA were further increased. GSTM1 may be one of the genetic risk factors for MWOA in the Japanese population.

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“…The role of the glutathione S -transferase (GST) detoxification enzymes (M1, P1 and T1) have been speculated in migraine susceptibility due to their chemical interactions with foods known to trigger migraine attacks [85] . The null genotype of the GSTM1 gene, resulting in no expression of the GSTM1 protein, was found not to be involved in a Swedish migraine cohort.…”

Section: Glutathione S-transferase Genesmentioning

confidence: 99%

A pharmacogenomic evaluation of migraine therapy

Johnson

Fernandez

Colson

et al. 2007

Expert Opinion on Pharmacotherapy

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Migraine is a common idiopathic primary headache disorder with significant mental, physical and social health implications. Accompanying an intense unilateral pulsating head pain other characteristic migraine symptoms include nausea, emesis, phonophobia, photophobia and in approximately 20-30% of migraine cases, neurologic disturbances associated with the aura phase. Although selective serotonin (5-HT) receptor agonists (i.e., 5-HT(1B/1D)) are successful in alleviating migrainous symptoms in < or = 70% of known sufferers, for the remaining 30%, additional migraine abortive medications remain unsuccessful, not tested or yet to be identified. Genetic characterization of the migrainous disorder is making steady progress with an increasing number of genomic susceptibility loci now identified on chromosomes 1q, 4q, 5q, 6p, 11q, 14q, 15q, 17p, 18q, 19p and Xq. The 4q, 5q, 17p and 18q loci involve endophenotypic susceptibility regions for various migrainous symptoms. In an effort to develop individualized pharmacotherapeutics, the identification of these migraine endophenotypic loci may well be the catalyst needed to aid in this goal. In this review the authors discuss the present treatment of migraine, known genomic susceptibility regions and results from migraine (genetic) association studies. The authors also discuss pharmacogenomic considerations for more individualized migraine prophylactic treatments.

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Cytochrome P450 2D6 and glutathione S‐transferase M1 genotypes and migraine

Abstract: The results of this study indicate that deficient metabolism because of mutated CYP2D6 alleles or GSTM1 allele variants is not important in the aetiology of migraine.

Cited by 11 publications

References 20 publications

Update on the genetics of migraine

Update on the genetics of migraine

Glutathione S-Transferase Polymorphisms: Susceptibility to Migraine without Aura

A pharmacogenomic evaluation of migraine therapy

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