Calcium channel mutations and migraine

Kors, Esther E.; Maagdenberg, Arn M. J. M. van den; Plomp, Jaap J.; Frants, Rune R.; Ferrari, Michel D.

doi:10.1097/00019052-200206000-00014

Cited by 34 publications

(16 citation statements)

References 47 publications

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“…FHM1 is an autosomal-dominant subtype of migraine with aura, caused by a spontaneous missense mutation in the CACNA1A gene encoding the ion-conducting, pore-forming α 1A subunit of (Ophoff et al 1996), combinations of FHM1 with various degrees of cerebellar ataxia (Ducros et al 2001, Ophoff et al 1996, or fatal coma due to excessive cerebral edema (Kors et al 2001(Kors et al , 2002.…”

Section: C2 Familial Hemiplegic Migraine Typementioning

confidence: 99%

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

Uchitel

Inchauspe

Urbano

et al. 2012

Journal of Physiology-Paris

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Section: C2 Familial Hemiplegic Migraine Typementioning

confidence: 99%

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

Uchitel

Inchauspe

Urbano

et al. 2012

Journal of Physiology-Paris

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“…Fourth, multiple genetic disorders with both strong characteristic similarities and high comorbidity with bipolar disorder (e.g., epilepsy, migraines) are known to be caused by any one of a number of ion channel or ion-transporting ATPase mutations (BahiBuisson et al 2007;Castro et al 2007;Chandy et al 2006;Dichgans et al 2005;Doering and Zamponi 2005;Fernandez et al 2008;Graves 2006;Grisar et al 1992;Kors et al 2002;Mossner et al 2005;Nappi et al 2000).…”

Section: Ion Channels and Related Regulatory Proteinsmentioning

confidence: 99%

Pathways-based analyses of whole-genome association study data in bipolar disorder reveal genes mediating ion channel activity and synaptic neurotransmission

2008

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Despite known heritability, the complex genetic architecture of bipolar disorder (likely including trait, locus and allelic heterogeneity, as well as genetic interactions) has confounded genetic discovery for many years. Even modern day whole genome association studies (WGAS) using over half a million common SNPs have implicated only a handful of genes at the genomewide level. Temporally coincident with this series of WGAS, a host of pathways-based analyses (PBAs) have emerged as novel computational approaches in the examination of large-scale datasets, but thus far rarely have been applied to WGAS data in psychiatric disorders. Here, we report a series of PBAs conducted using exploratory visual analysis, an analytic and visualization software tool for examining genomic data, to examine results from the National Institutes of Mental Health and Wellcome-Trust Case Control Consortium WGAS in bipolar disorder. Consistent with a host of prior linkage findings, some candidate gene association studies, and recent WGAS, our strongest findings suggest involvement of ion channel structural and regulatory genes, including voltage-gated ion channels and the broader ion channel group that comprises both voltage- and ligand-gated channels. Moreover, we found only modest overlap in the particular genes driving the significance of these gene sets across the analyses. This observation strongly suggests that variation in ion channel genes, as a class of genes, may contribute to the susceptibility of bipolar disorder and that heterogeneity may figure prominently in the genetic architecture of this susceptibility.

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“…More generally, the role of FHM genes codifying for neuronal channels as Cav 2 .1, Na v 1, Na + and K + -ATPase at the cerebral level constitute a possible object of pharmacogenomic research [19]. …”

Section: Familial Hemiplegic Migraine a Mendelian Model For Migrainementioning

confidence: 99%

Genetics of migraine and pharmacogenomics: some considerations

Piane

Lulli

Farinelli³

et al. 2007

J Headache Pain

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Migraine is a complex disorder caused by a combination of genetic and environmental factors.Although family and twin studies show that there is a genetic component in migraine, no genes predisposing to common forms of the disorder, migraine with and without aura, have been identified. Patients with migraine respond differently to a given drug administered. The efficacy of therapy and the occurrence of adverse drug response are a consequence of individual variability. Genetic profiling of predisposition to migraine should facilitate the development of more effective diagnostic and therapeutic applications. The development of International Hap Map project could provide a powerful tool for identification of the candidate genes in this complex disease and pharmacogenomics research could be the promise for individualized treatments and prevention of adverse drug response.

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Calcium channel mutations and migraine

Cited by 34 publications

References 47 publications

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis

Pathways-based analyses of whole-genome association study data in bipolar disorder reveal genes mediating ion channel activity and synaptic neurotransmission

Genetics of migraine and pharmacogenomics: some considerations

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