A Polymorphism in the Interleukin‐1α Gene Influences the Clinical Features of Migraine

Rainero, Innocenzo; Pinessi, Lorenzo; Salani, Giuliana; Valfrè, Walter; Rivoiro, Chiara; Savi, L; Gentile, Salvatore; Giudice, R Lo; Grimaldi, Luigi Maria Edoardo

doi:10.1046/j.1526-4610.2002.02103.x

Cited by 26 publications

(16 citation statements)

References 17 publications

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“…However, subsequent reports have not confirmed an association, as has often been the case with this method of analysis (Lea et al 2000;Maude et al 2001). Other genes with suggested polymorphisms associated with migraine include glutathione-S-transferase/GST (MO; Kusumi et al 2003), dopamine receptor type 4/DRD4 (MO; Mochi et al 2003), TNF-β /lymphotoxin alpha (MO; Trabace et al 2002), interleukin 1A/IL-1A (Rainero et al 2002b), serotonin transporter (Yilmaz et al 2001), the C677T methyl-tetrahydrofolate reductase allele/MTHFR (Kowa et al 2000), the dopamine beta hydroxylase gene/DBH (Lea et al 2000), angiotensin-converting enzyme-DD allele/ACE-DD (Paterna et al 2000), ABO to alpha-1-antitrypsin among group components (Chr4; Pardo et al 1995), and esterase-D (Chr13; Pardo et al 1995).…”

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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“…An IL1A single-nucleotide polymorphism (SNP), IL1A À889 C to T, has been associated with myasthenia gravis, 17 sarcoidosis, 18 age of onset of migraine 19 and juvenile rheumatoid arthritis. 20 Two SNPs in IL1B have reported genetic associations with disease.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1 gene cluster polymorphisms and susceptibility to clinical malaria in a Gambian case–control study

et al. 2003

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Interleukin-1 (IL1) is a potent endogenous pyrogen and inducer of the acute phase response, and these innate immune responses are an important part of the human host's initial reaction to infection by the malaria parasite. In addition, several single-nucleotide polymorphisms (SNPs) in this region have previously been demonstrated to be associated with susceptibility to infectious disease. Therefore, a possible association with malaria susceptibility was investigated. A total of 13 polymorphic markers were used in a two-stage screening strategy to genotype a Gambian case -control study group by either restriction endonuclease digestion or the Sequenom MassARRAYt assay. This involved an initial screen of 188 severe cases and 188 mild controls, and if there was a significant association with a malaria phenotype (Po0.05); this was followed by screening of the remaining 1044 samples. Two markers showed significant association with malaria: interleukin-1 alpha þ 4845 G-T (P ¼ 0.035 for mild malaria versus controls) and interleukin-1 beta þ 3953 C-T (P ¼ 0.030 for mild malaria versus severe malaria). Haplotypes constructed using the SNPHAP programme were not associated with any of the malaria phenotypes investigated. In summary, if IL1 variants are involved in malaria susceptibility in the Gambia at all, then the effects are small.

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“…The same group had previously observed a protective role for the HLA-DR2 antigen in MA [68]. Finally, a polymorphism in the interleukin-1alpha gene was found to influence age at onset of migraine and was associated with MA [69].…”

Section: Migraine and Genes Involved In Inflammationmentioning

confidence: 68%

The “typical” migraines: genetic studies and some practical considerations

2003

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"Typical" migraine as a complex disease: genetic epidemiology, twin and segregation analysis studies That migraine runs in families is an ancient observation. Familiarity however is not synonymous with heritability, especially given the wide prevalence of migraine and the possibility that familial occurrence is due to chance. In order to assess the heritability of migraine, e.g. the rate of variance attributable to genetic factors, the disease risk of relatives of migraine probands is determined and compared to that found in the general population. Several surveys indicated that first-and sometimes also seconddegree relatives of migraine probands show increased risk for migraine: a two-fold increased risk for migraine without aura (MO) and 1.4 for migraine with aura (MA) in the case of first-degree relatives of MO probands, and a 4-fold risk for MA in the case of first-degree relatives of MA probands [1]. An increased disease risk does not however prove heritability, since it may result from shared environmental factors. It is therefore interesting to note that at least one genetic epidemiology survey found an increased disease risk for migraine in first-degree relatives compared to spouses of migraine probands, who presumably share environmental factors at least for some time in their lives. Notably however, the relative risk for spouses was increased compared to the general population, which implies some degree of assorted mating or shared environmental influences [1]. Studies of heritability performed according to disease risk comparisons came to high rates of genetic determination, e.g. 60%-80% for MO and MA [2].Better ways of analysing heritability of migraine are studies of monozygotic versus dizygotic twins, especially when reared-together and reared-apart (adopted) identical twins are considered. Several twin studies have been performed in migraine Pasquale Montagna Pietro Cortelli Mirella MochiAbstract Epidemiological genetic, family and twin studies show that the typical migraines carry a substantial genetic risk; they are currently conceptualized as complex genetic diseases. Several genetic association and linkage studies have been performed in the typical migraines. Candidate gene studies based on "a priori" pathogenic models of migraine (migraine as a calcium channelopathy; a mitochondrial DNA disorder; a disorder in the metabolism of serotonin or dopamine; in vascular risk factors or in the inflammation cascade; etc.) did not result in uniformely accepted findings. Linkage and genome wide scans gave evidence for several genetic susceptibility loci, still however in need of confirmation. Careful dissection of the clinical phenotypes and trigger factors shall greatly help future efforts in the quest for the genetic basis of the typical migraines.

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A Polymorphism in the Interleukin‐1α Gene Influences the Clinical Features of Migraine

Abstract: The results of our study suggest a role for the IL1A gene in modifying the clinical features of migraine.

Cited by 26 publications

References 17 publications

Update on the genetics of migraine

Update on the genetics of migraine

Interleukin-1 gene cluster polymorphisms and susceptibility to clinical malaria in a Gambian case–control study

The “typical” migraines: genetic studies and some practical considerations

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