Deficiency of Tumor Necrosis Factor <b>α</b> in a Subclass of Menstrual Migraineurs

Mueller, Loretta; Gupta, Adarsh; Stein, T. P.

doi:10.1046/j.1526-4610.2001.111006129.x

Cited by 38 publications

(35 citation statements)

References 30 publications

(66 reference statements)

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“…Further, lower serum concentrations of the soluble receptor for TNF-alpha have been reported in migraineurs compared to controls, while the serum concentrations of TNF-alpha did not differ (9). In contrast, among women with menstrual migraine urine secretion of TNF-alpha appears to be markedly decreased (8). Second, TNF-alpha was shown to stimulate CGRP gene transcription and CGRP plays a key role in the pathophysiology of migraine (10).…”

Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor gene polymorphisms and migraine: A systematic review and meta-analysis

et al. 2011

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Background Data on the association between TNF-alpha and TNF-beta gene polymorphisms and migraine are conflicting. Methods We performed a systematic review and meta-analysis of studies published until January 2011. We used data from published papers and as provided after contact with the authors. We calculated study specific odds ratios (OR) and 95% confidence intervals (CI) assuming additive, dominant, and recessive genetic models as well as pooled effect estimates. Results Among the ten studies identified the best evidence is available for the TNF-alpha -308G>A and TNF-beta 252A>G polymorphisms indicating no overall association with migraine. Subgroup analyses suggested that the A allele of the TNF-alpha -308G>A variant more than doubles the risk for migraine among populations with a heterogeneous ethnic background, which was driven by associations for MO (additive model: pooled OR=2.87; 95% CI 1.86–4.43). Further, the risk for MA was increased among Asian populations (additive model: pooled OR=1.71; 95% CI 1.07–2.71). Both observed effects were stronger among females than males. Conclusions Our results indicate no overall association between TNF-alpha and TNF-beta gene variants. However, associations differed among specific populations. Our findings need to be treated with caution and further targeted research is warranted to evaluate population-specific effects including population stratification.

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Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor gene polymorphisms and migraine: A systematic review and meta-analysis

et al. 2011

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“…Inflammatory and immune mediators, including TNF-α, IL-1, CGRP, orexin, and IL-6, are involved in migraine pathogenesis, and substance P, CGRP, and IL-6 are elevated during acute migraine attacks (Jang et al, 2010). TNF-α is a proinflammatory molecule produced by excess adipose tissue (Rönnemaa et al, 2000) and serum TNF-α levels are elevated in menstrual migraine (Mueller et al, 2001). The gain of function TNF-α-308 A and IL-1β + 3953 T allele gene polymorphisms are elevated in patients with migraine without aura (Yilmaz et al, 2010), although the implications are unclear.…”

Section: Migraine and Obesitymentioning

confidence: 99%

Metabolic Syndrome and Migraine

Sachdev¹,

Marmura²

2012

Front. Neur.

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Migraine and metabolic syndrome are highly prevalent and costly conditions. The two conditions coexist, but it is unclear what relationship may exist between the two processes. Metabolic syndrome involves a number of findings, including insulin resistance, systemic hypertension, obesity, a proinflammatory state, and a prothrombotic state. Only one study addresses migraine in metabolic syndrome, finding significant differences in the presentation of metabolic syndrome in migraineurs. However, controversy exists regarding the contribution of each individual risk factor to migraine pathogenesis and prevalence. It is unclear what treatment implications, if any, exist as a result of the concomitant diagnosis of migraine and metabolic syndrome. The cornerstone of migraine and metabolic syndrome treatments is prevention, relying heavily on diet modification, sleep hygiene, medication use, and exercise.

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“…Tumor necrosis factor-alpha (TNF-alpha) is an important inflammatory cytokine and modulator of immune responses. Its role in migraine has been postulated based on reports of TNF-alpha concentration changes in serum [29–31] and urine [32] among migraineurs, as well as findings that TNF-alpha can stimulate transcription of calcitonin gene-related peptide (CGRP), which is pivotal in migraine pathophysiology [33]. Variants in the genes coding for TNF-alpha and the closely related TNF-beta have been shown to modulate cytokine levels of TNF-alpha and TNF-beta [34, 35] prompting investigations of various polymorphisms in these genes with respect to their role in migraine.…”

Section: Candidate Gene Approachesmentioning

confidence: 99%

Genetics of migraine in the age of genome-wide association studies

Schürks

2011

J Headache Pain

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Genetic factors importantly contribute to migraine. However, unlike for rare monogenic forms of migraine, approaches to identify genes for common forms of migraine have been of limited success. Candidate gene association studies were often negative and positive results were often not replicated or replication failed. Further, the significance of positive results from linkage studies remains unclear owing to the inability to pinpoint the genes under the peaks that may be involved in migraine. Problems hampering these studies include limited sample sizes, methods of migraine ascertainment, and the heterogeneous clinical phenotype. Three genome-wide association studies are available now and have successfully identified four new genetic variants associated with migraine. One new variant (rs1835740) modulates glutamate homeostasis, thus integrates well with current concepts of neurotransmitter disturbances. This variant may be more specific for severe forms of migraine such as migraine with aura than migraine without aura. Another variant (rs11172113) implicates the lipoprotein receptor LRP1, which may interact with neuronal glutamate receptors, thus also providing a link to the glutamate pathway. In contrast, rs10166942 is in close proximity to TRPM8, which codes for a cold and pain sensor. For the first time this links a gene explicitly implicated in pain related pathways to migraine. The potential function of the fourth variant rs2651899 (PRDM16) in migraine is unclear. All these variants only confer a small to moderate change in risk for migraine, which concurs with migraine being a heterogeneous disorder. Ongoing large international collaborations will likely identify additional gene variants for migraine.

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Deficiency of Tumor Necrosis Factor α in a Subclass of Menstrual Migraineurs

Abstract: This deficiency of TNF-alpha levels in women with migraine may signal a disordered neuroimmune communication network and predisposition to migraine.

Cited by 38 publications

References 30 publications

Tumour necrosis factor gene polymorphisms and migraine: A systematic review and meta-analysis

Tumour necrosis factor gene polymorphisms and migraine: A systematic review and meta-analysis

Metabolic Syndrome and Migraine

Genetics of migraine in the age of genome-wide association studies

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