Searching for migraine genes: exclusion of 290 cM out of the whole human genome

Monari, L.; Mochi, M.; Valentino, Maria Lucia; Arnaldi, C.; Cortelli, Pietro; Monte, A. De; Pierangeli, Giulia; Prologo, G.; Scapoli, Chiara; Soriani, Stefano; Montagna, Pasquale

doi:10.1007/bf02083304

Cited by 33 publications

(20 citation statements)

References 16 publications

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“…The only study to report a significant association with migraine involved genetic variants of the 5-HT transporter SERT gene, in which an overrepresentation of allele Stin2.12 and a reduction of allele Stin2.10 were found in MO, with an additional trend to overrepresented Stin 2.9 allele in MA [39]. Exactly the opposite (increased Stin2.10 allele in migraine) was found by Yilmaz et al [40], however, and negative findings were reported both by us in our sample of 14 Italian families with migraine [15] and by Lea et al [41].…”

Section: Migraine and The Mitochondrial Genomecontrasting

confidence: 51%

“…They excluded a region of 50 cM, flanking the FHM locus as a site of migraine liability. In our own study of 14 Italian families with MO and MA, we performed association, linkage and sib-pair analyses to markers near the CACNA1A region, with negative results [15]. In another study of Italian familial cases of "complicated" migraine, migraine stroke and MA [16], we reported the absence of the four original CACNA1A mutations described in FHM by Ophoff et al [17].…”

Section: Migraine As a Channelopathymentioning

confidence: 99%

“…However, the genetic evidence is murky, since positive studies of association with dopamine receptors genes, in particular DRD2, have been contradicted in other populations. NcoIC allele of the DRD2 gene was found associated with MA, and in particular with MA co-morbid with anxiety and depression, by Allelic association with migraine (increased Stin 2.10 allele) [40] No association or linkage with migraine [15,41] 5-HT2A (13q14-21) Allelic association (C allele) with aura but not with migraine [42] No [23] MtDNA deletion in 1 case with migraine stroke Shimomura et al (1995) [35] 11084 mtDNA mutation in 25% of 53 Japanese migraineurs Ojaimi et al (1998) [32] 4216 and 13708 LHON secondary mutations in juvenile stroke Majamaa et al (1997) [31] MELAS mutation in 6% of juvenile migraine stroke Majamaa et al (1998) [29] MtDNA U haplotype in migraine stroke Finnila et al (2001) [33] MtDNA U5 haplotype and tRNA mutations in migraine stroke Ohno et al (1998) [36] tRNA Glu and 12SrRNA mutations in matrilinear FHM Shimomura et al (1994) [37] tRNA Leu UUR mutation in cluster headache Odawara et al (1997) [38] mtDNA deletion in cluster headache Boles et al (1999) [34] 8.1 kb mtDNA deletion in cyclic vomiting syndrome Allelic association (NcoI allele) with MA co-morbid with [49] anxiety/depression Allelic association (allele 1) with yawning/nausea during MO attack [50] No allelic (NcoI allele) association with MA [51] No allelic association with MO/MA [52] No allelic association with migraine [41] …”

Section: Migraine and Dopamine Metabolism Genesmentioning

confidence: 99%

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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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Section: Migraine and The Mitochondrial Genomecontrasting

confidence: 51%

Section: Migraine As a Channelopathymentioning

confidence: 99%

Section: Migraine and Dopamine Metabolism Genesmentioning

confidence: 99%

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

2003

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“…However, an attempt to identify the chromosomal locations of the candidate genes 5-HT 1D (1p36.3-34.3), 5-HT 1B (6p13), 5-HT 2A (13q14-21), 5-HT transporter (17q11.2-12), CACNLB1 (17q11. and FHM locus (19p13) was failed [24] .The 11084 A to G base substitution was not confirmed to be the gene for the ND4 subunit of respiratory complex 1 as found in 25% of Japanese migraineurs [25] and the mutation of this gene was not associated with the migraine in Denmark. No differences or trends in allele or genotype frequencies of 5-HT 2C receptor gene were found in migraineurs [9] .…”

Section: Genes Associated With Migrainementioning

confidence: 91%

Migraine as a sex-conditioned inherited disorder: evidences from China and the world

et al. 2008

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Migraine is a complex and heterogeneous disorder. Although several genetic models has been proposed including autosomal-dominant/autosomal recessive, sex-linked, sex-limited, mitochondrial, and multi-gene, none of these models can well-explain the transmission of the disease. We hypothesied that migraine is a sex-conditioned inherited disorder (autosomal dominant in females and autosomal recessive in males). This hypothesis is supported by the evidence such as the locations of genes associated with familial hemiplegic migraine, possibly "typical" migraine as well (dominantly on chromosome 19p, 1q, and 2q), male:female ratio of prevalence (1:2-1:4), the mostly youth-onset, the provocation by the contraceptives, the induction by menstruation, and the self-limitation after menopause. Female sex-hormones appear to be the key contributor to a higher prevalence of migraine in female. Socio-environmental factors may also play an important role.

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“…Linkage studies have predictably proved negative [20]. Surprisingly, in view of the female preponderance of migraine, Nyholt et al [19] identified a linkage with the X chromosome (Xq24-28) in 2 families.…”

Section: Familial Hemiplegic Migrainementioning

confidence: 99%

The genetics of migraine

Montagna

2001

J Headache Pain

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Migraine is currently considered to be a multifactorial disease in that it is modified by environmental and genetic factors and has a polygenic determination. Familial hemiplegic migraine (FHM), a subtype of migraine with aura conforming to simple mendelian transmission, has been shown to result from mutations in the CACNA1A gene, a neural calcium channel gene. FHM is allelic with episodic ataxia type 2 and spinocerebellar ataxia type 6. FHM is genetically heterogeneous, with at least another linkage locus on chromosome 1. Association and linkage studies have also been performed in migraine with and without aura, the so–called typical migraines, without however definite results up to now.

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Searching for migraine genes: exclusion of 290 cM out of the whole human genome

Cited by 33 publications

References 16 publications

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

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

Migraine as a sex-conditioned inherited disorder: evidences from China and the world

The genetics of migraine

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