Migraine and Genetic and Acquired Vasculopathies

Stam, AH; Haan, Joost; Maagdenberg, Amjm van den; Ferrari, Michel D.; Terwindt, G.M.

doi:10.1111/j.1468-2982.2009.01940.x

Cited by 62 publications

(52 citation statements)

References 113 publications

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“…3,5,6 Pathophysiology linking these neurovascular disorders remains poorly understood; suggested mechanisms include cortical spreading depression, 7 endothelial dysfunction, 8 enhanced platelet activation, 9 and vasoconstriction. …”

Section: Discussionmentioning

confidence: 99%

Shared genetic basis for migraine and ischemic stroke

Malik¹,

Freilinger²,

Winsvold³

et al. 2015

Neurology

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Objective: To quantify genetic overlap between migraine and ischemic stroke (IS) with respect to common genetic variation. Methods:We applied 4 different approaches to large-scale meta-analyses of genome-wide data on migraine (23,285 cases and 95,425 controls) and IS (12,389 cases and 62,004 controls). First, we queried known genome-wide significant loci for both disorders, looking for potential overlap of signals. We then analyzed the overall shared genetic load using polygenic scores and estimated the genetic correlation between disease subtypes using data derived from these models. We further interrogated genomic regions of shared risk using analysis of covariance patterns between the 2 phenotypes using cross-phenotype spatial mapping. Results:We found substantial genetic overlap between migraine and IS using all 4 approaches.Migraine without aura (MO) showed much stronger overlap with IS and its subtypes than migraine with aura (MA). The strongest overlap existed between MO and large artery stroke (LAS; p 5 6.4 3 10 228 for the LAS polygenic score in MO) and between MO and cardioembolic stroke (CE; p 5 2.7 3 10 220 for the CE score in MO). Conclusions:Our findings indicate shared genetic susceptibility to migraine and IS, with a particularly strong overlap between MO and both LAS and CE pointing towards shared mechanisms. Our observations on MA are consistent with a limited role of common genetic variants in this subtype. Neurology ® 2015;84:2132-2145 GLOSSARY CE 5 cardioembolic stroke; CPSM 5 cross-phenotype spatial mapping; GWAS 5 genome-wide association studies; IHGC 5 International Headache Genetics Consortium; IS 5 ischemic stroke; LAS 5 large artery stroke; LD 5 linkage disequilibrium; MA 5 migraine with aura; MO 5 migraine without aura; SNP 5 single nucleotide polymorphism; SVD 5 small vessel disease.Migraine is a primary headache disorder characterized by recurrent attacks of severe, often throbbing, headache associated with autonomic dysfunction. Although the majority of patients have migraine without aura (MO), one third have headaches preceded by transient neurologic disturbances (migraine with aura [MA]). 1 Ischemic stroke (IS) is etiologically heterogeneous and a leading cause of premature death and disability. Results of epidemiologic studies show increased risk of IS in migraine patients.3 A large metaanalysis of case-control and observational cohort studies reported an increased risk of IS for patients with MO and MA, 4 whereas more recent meta-analyses reported the association to be restricted to MA. 3,5,6 Pathophysiology linking these neurovascular disorders remains poorly understood; suggested mechanisms include cortical spreading depression, 7 endothelial dysfunction, 8 enhanced platelet activation, 9 and vasoconstriction.

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Section: Discussionmentioning

confidence: 99%

Shared genetic basis for migraine and ischemic stroke

Malik¹,

Freilinger²,

Winsvold³

et al. 2015

Neurology

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“…Pre-eclampsia is itself associated with pre-term birth, perinatal death 3 and with infant stroke in the perinatal period, 24 and also with risk of maternal pregnancy-associated stroke 7 and with long-term stroke risk in the mother. 4 In preeclampsia, 25,26 as in migraine, 27,28 there are features of endothelial dysfunction, platelet activation and inflammation.…”

Section: Migraine and Preterm Birthmentioning

confidence: 99%

Migraine and preterm birth

Blair

Nelson

2010

J Perinatol

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Objective: To investigate whether maternal migraine was associated with preterm birth.Study Design: Case-control sample within a population-based study of risk factors for cerebral palsy (CP). Infants without CP were matched for gestational age with those with CP. Maternal migraine was self-identified at first prenatal visit, most in the first trimester.Result: Infants without CP born to women with migraine had a higher rate of preterm birth (odds ratio (OR) ¼ 3.5, 95% confidence interval (CI) 1.5, 8.5), as did infants who died in the perinatal period (OR ¼ 7.3, 95% CI 0.98, 54), the difference marginal for nominal statistical significance. In all outcome groups, infants of women with migraine had a higher observed rate of suboptimal intrauterine growth. In term infants, the rate of maternal migraine was higher in those with CP than in controls (OR ¼ 2.18, 95% CI 0.92, 5.25). Pre-eclampsia was reported more frequently in women with migraine who gave birth to a child with CP or a perinatal death, particularly in those born preterm; OR ¼ 5.1 (1.3, 20) and OR ¼ 2.9 (1.1, 7.6), respectively, but not in women giving birth to a control whether term or preterm.Conclusion: Maternal migraine, as self-reported early in pregnancy, was associated with preterm birth in survivors without CP and in infants who died in the perinatal period. The combination of maternal migraine and pre-eclampsia was associated with CP and perinatal death. The association of maternal migraine with outcomes of pregnancy warrants further study.

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“…The discovery that TREX1 mutations cause Aicardi-Goutières syndrome (AGS) 3 provides an important link between nucleic acid metabolism, autoimmune disease, and innate antiviral response (5). The additional findings of TREX1 mutations in patients diagnosed with familial chilblain lupus, Cree encephalitis, retinal vasculopathy with cerebral leukodystrophy (RVCL), and systemic lupus erythematosus (SLE) genetically link a spectrum of human autoimmune disorders with overlapping related clinical symptoms (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

mentioning

confidence: 99%

The TREX1 C-terminal Region Controls Cellular Localization through Ubiquitination

Orebaugh

Fye

Harvey

et al. 2013

Journal of Biological Chemistry

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Background: Mutations in the TREX1 C-terminal region (CTR) cause human autoimmune disease. Results: The CTR directs TREX1 ubiquitination and interaction with ubiquilin 1. Conclusion: TREX1 ubiquitination and co-localization with ubiquilin 1 are differentially affected in autoimmune disease mutants. Significance: Multiple mechanisms of TREX1 dysfunction include altered covalent modification and diminished catalytic function, resulting in a spectrum of autoimmune diseases.

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Migraine and Genetic and Acquired Vasculopathies

Cited by 62 publications

References 113 publications

Shared genetic basis for migraine and ischemic stroke

Shared genetic basis for migraine and ischemic stroke

Migraine and preterm birth

The TREX1 C-terminal Region Controls Cellular Localization through Ubiquitination

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