Significance of serotonin transporter gene polymorphism in migraine

Yılmaz, Mustafa; Erdal, Mehmet Emin; Herken, Hasan; Çataloluk, Osman; Barlas, İbrahim Ömer; Bayazıt, Yıldırım A.

doi:10.1016/s0022-510x(01)00491-9

Cited by 67 publications

(86 citation statements)

References 13 publications

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“…The polymorphism of the VNTR region in the 5-HTT was shown to be associated with myofacial pain syndrome and migraine as well [49,31]. To our knowledge, the VNTR polymorphism has not been investigated in ADHD to date.…”

Section: Discussionmentioning

confidence: 95%

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Significance of Serotonin Transporter Gene 5-HTTLPR and Variable Number of Tandem Repeat Polymorphism in Attention Deficit Hyperactivity Disorder

Zoroğlu

Erdal²,

Alaşehirli³

et al. 2002

Neuropsychobiology

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The purpose of this study was to evaluate the relationship between attention deficit hyperactivity disorder (ADHD) and polymorphism of the two regions of the 5-HTT gene [variable number of tandem repeats (VNTR) and 5-HTTLRR] in a sample of Turkish children. Using the PCR technique, these polymorphisms were assessed in 71 patients with ADHD and 128 healthy controls. The 5-HTTLPR S/S genotype was significantly lower in the patients than in the controls (p = 0.018). Homozygous and heterozygous L variant predominated in the ADHD group. But the VNTR STin2.12/12 genotype was significantly less found in the patients than in the controls (p = 0.001). There was no significant difference between the frequency of the short (S), long, 10, and 12 alleles of both groups. The lack of an S/S variant of 5-HTTLPR polymorphism of the STin2.12/12 variant of VNTR polymorphism appears to be associated with an increased risk of ADHD.

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Section: Discussionmentioning

confidence: 95%

“…Amplification products were resolved by electrophoresis on 2% agarose gels next to a DNA molecular weight standard and visualized with ethidium bromide staining. Alleles were designated 390 bp (12 copies, STin2.12), 360 bp (10 copies, STin2.10) or 345 bp (9 copies, STin2.9) as described previously [31].…”

Section: Methodsmentioning

confidence: 99%

Significance of Serotonin Transporter Gene 5-HTTLPR and Variable Number of Tandem Repeat Polymorphism in Attention Deficit Hyperactivity Disorder

Zoroğlu

Erdal²,

Alaşehirli³

et al. 2002

Neuropsychobiology

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“…Anxiety and depression symptoms are often comorbid to tinnitus, and are affected from serotonin and GABA receptors. [16].…”

Section: Discussionmentioning

confidence: 99%

Does Tinnitus Lead to Depression?

Temügan¹,

Yildirım²,

Onat³

et al. 2016

CIM

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Purpose: The aim of the study was to investigate the correlation between THI (Tinnitus Handicap Inventory) and BDS (Beck Depression Scale). Materials and Methods:High frequency thresholds and PTA (Pure Tone Audiometer) thresholds for the patients were measured in 44 patients with tinnitus (bilateral=13; unilateral=31). Tinnitus frequency and intensity were measured using one-pair method with high frequency audiometer Interacoustic AC40. Applied BDS and THI scores are evaluated for all patients. Our findings are analysed statistically with SPSS v.21 and BDS and THI correlation with tinnitus intensity and frequency was executed.Results: The mean value of tinnitus frequency was 10 kHz (min 0.25 kHz, max16 kHz and SD 4.26), mean tinnitus intensity was 50.6 dB (min 15 dB, max 110 dB and SD 26.9 dB) mean THI score was 38.04 (min 10, max 86 and SD 20.03) and mean BDS score was 9.45 (min 0, max 28 and SD 6.49). There was no statistical correlation between THI score and tinnitus frequency (r=0.055, p=0.787). Moderate correlation is obtained between tinnitus frequency and depression (r=0.6, p=0.001). There were weak correlations between tinnitus intensity and THI score and (r=0.3, p=0.09) and between tinnitus intensity and BDS score (r=0.28, p=0.13). Although a statistically significant difference was observed between THI scores of patients with bilateral and unilateral tinnitus (p<0.05), BDS scores of these groups were not statistically different from each other (p>0.05). High frequency thresholds and UCL scores of ears with tinnitus were not statistically different from ears with no tinnitus (p>0.05). Conclusion:No correlation was seen between THI and tinnitus frequency, but a moderate correlation was seem between BDS score and tinnitus frequency. There were also weak correlations between tinnitus intensity and THI and BDS scores.SUPPLEMENT

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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 Genomementioning

confidence: 92%

“…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%

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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Significance of serotonin transporter gene polymorphism in migraine

Cited by 67 publications

References 13 publications

Significance of Serotonin Transporter Gene 5-HTTLPR and Variable Number of Tandem Repeat Polymorphism in Attention Deficit Hyperactivity Disorder

Significance of Serotonin Transporter Gene 5-HTTLPR and Variable Number of Tandem Repeat Polymorphism in Attention Deficit Hyperactivity Disorder

Does Tinnitus Lead to Depression?

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

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