Tumor Necrosis Factor Gene Polymorphism in Migraine

Trabace, S; Brioli, Gloria; Lulli, Patrizia; Morellini, M; Giacovazzo, M; Cicciarelli, Germana; Martelletti, Paolo

doi:10.1046/j.1526-4610.2002.02104.x

Cited by 58 publications

(71 citation statements)

References 27 publications

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“…Transitory increases in the levels of TNFa have been observed in the plasma of migraineurs (22 MO, 4 MA) [Perini et al, 2005] and in the internal jugular blood of migraineurs with aura [Sarchielli et al, 2006] during an attack. Analysis of TNFb polymorphisms suggested a role for TNFb in MO but not in MA [Trabace et al, 2002]. In a separate study, investigation of TNFa also showing an association with MO but not MA .…”

Section: Other Genesmentioning

confidence: 84%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

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Migraine is a common complex neurological disorder with a well-known but poorly characterized genetic liability. The search for migraine susceptibility genes has been the focus of intense research. It is now believed that common migraine is not a single gene disorder, but attributable to several potentially interacting genetic variants. These variants may differ in each sufferer and interact with environmental factors to set the individual migraine threshold. This genetic liability may play an important role in the clinical heterogeneity seen in migraine and also in the variability of treatment response. This review will look at genetic loci implicated in migraine to date and consider their current or prospective role in migraine therapy. To elucidate the complex nature of migraine genetic liability, approaches that consider detailed endophenotypic profiles that encompass treatment response may provide much more relevant information than simple end diagnosis. Drug Dev Res 68: 282-293, 2007. r 2007 Wiley-Liss, Inc.

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Section: Other Genesmentioning

confidence: 84%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

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“…In case of CSD (cortical spreading depression), for example, this process causes a local neurogenic inflammation with the activation of mast cells and macrophages, accompanied by the release of pro-inflammatory cytokines, ultimately leading to sensitization of meningeal nociceptive nerve endings [94]. For the COX-2, HLA-DRB1, LTA, TNFA, TNFB and TNFRSF1B genes, positive associations with migraines were detected [95][96][97][98][99][100][101][102].…”

Section: Inflammation and Genesmentioning

confidence: 99%

Genetics of Migraine - Is There any Progress?

Klimov¹,

Kondratieva²,

Анучина³

et al. 2017

JNSK

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Nowadays migraine ranks 9th in the list of leading causes of disability among population. In Russia migraine prevalence is two times higher than the world index and inflicts a considerable damage on the state economy. Despite almost one-century history of studying migraine, science until now cannot explain many cases of attack occurrence. It causes difficulties both for diagnosis and treatment -the therapy of patients with migraine is not sufficiently effective. Today one of the investigation directions is searching of migraine biomarkers confirming diagnosis. In this review we attempted to generalize the results of available works targeted at searching genetic markers of migraine.

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“…Peroutka et al [54] studied polymorphism frequencies for complement C3F and C3S in a sample of 137 migraineurs and found that this common polymorphism had no association with migraine susceptibility. Trabace et al [67] found that the frequency of TNFB*2 allele, located in the HLA class III region, was significantly increased and that of TNFB1 decreased in MO, suggesting that the TNFB*2 allele confers a high risk for MO. The same group had previously observed a protective role for the HLA-DR2 antigen in MA [68].…”

Section: Migraine and Genes Involved In Inflammationmentioning

confidence: 99%

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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Tumor Necrosis Factor Gene Polymorphism in Migraine

Abstract: These data support the hypothesis that lymphotoxin alpha could be a susceptibility gene in migraine without aura and confirm previous data indicating that migraine with and without aura are distinct entities with different genetic backgrounds.

Cited by 58 publications

References 27 publications

Migraine genetics and prospects for pharmacotherapy

Migraine genetics and prospects for pharmacotherapy

Genetics of Migraine - Is There any Progress?

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

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