Genetics Research
rs3742278
Population Frequencies12
African
A 0.74451G 0.25549AA 0.555827AG/GA 0.377361GG 0.066813pop=55,708
African American
A 0.74577G 0.25423AA 0.557766AG/GA 0.376009GG 0.066225pop=53,786
African Others
A 0.7092G 0.2908AA 0.501561AG/GA 0.415193GG 0.083247pop=1,922
Asian
A 0.52029G 0.47971AA 0.274403AG/GA 0.491782GG 0.233814pop=13,994
East Asian
A 0.49483G 0.50517AA 0.244372AG/GA 0.500908GG 0.25472pop=11,016
European
A 0.865425G 0.134575AA 0.749039AG/GA 0.232772GG 0.018189pop=513,378
Latin American 1
A 0.82335G 0.17665AA 0.677784AG/GA 0.291125GG 0.031091pop=10,614
Latin American 2
A 0.78062G 0.21938AA 0.607472AG/GA 0.346291GG 0.046237pop=18,470
Other
A 0.80465G 0.19535AA 0.64889AG/GA 0.311513GG 0.039597pop=17,476
Other Asian
A 0.6145G 0.3855AA 0.385494AG/GA 0.458026GG 0.156481pop=2,978
South Asian
A 0.8218G 0.1782AA 0.679712AG/GA 0.284243GG 0.036045pop=3,884
Studies24
Unread Studies24 ▼
1
Social anxiety disorder (SAD) is a common psychiatric disorder, often associated with avoidant temperament. Research studies have implicated a strong genetic architecture of SAD. We have conducted a systematic review on the genetics of SAD and yielded 66 articles. In general, prior research studies have focused on the serotonin transporter, oxytocin receptor, brain-derived neurotrophic factor and catechol-O-methyltransferase genes. Mixed and inconsistent results have been reported. Additional approaches and phenotypes have also been investigated, including pharmacogenetics of treatment response, imaging genetics and gene-environment interactions. Future directions warrant further international collaborative efforts, deep-phenotyping of clinical characteristics including consistent and reliable measurement-based symptom severity, and larger sample sizes to ensure sufficient power for stratification due to the heterogeneity of this chronic and often debilitating condition.
2
Serotonin genes are commonly studied in obsessive-compulsive disorder (OCD), but findings have been inconsistent. OCD is phenotypically heterogeneous, with …
3
Serotonin system genes are commonly studied in obsessive‐compulsive disorder ( OCD ), but genetic studies to date have produced inconsistent results, possibly because …
4
Serotonin system genes are commonly studied in obsessive-compulsive disorder (OCD), but genetic studies to date have produced inconsistent results, possibly because phenotypic heterogeneity has not been adequately accounted for. In this paper, we studied candidate serotonergic genes and homogenous phenotypic subgroups as presented through obsessive-compulsive (OC) trait dimensions in a general population of children and adolescents. We hypothesized that different serotonergic gene variants are associated with different OC trait dimensions and, furthermore, that they vary by sex.
5
OF ESTABLISHING A GENETIC RISK STRATIFICASTION FOR GENETIC ADDICTION RISK ANALYSIS - Patent application Patents - stay tuned to the technology Inventors …
6
ssing severity index for alcohol abuse, drug abuse, and other reward deficiency syndromes. It has been discovered that a multifaceted non-specific RDS behaviors should be …
7
Purpose of review The present review aims to deliver a systematic overview of current developments and trends in (epi)genetics of anxiety and to identify upcoming challenges and opportunities. Recent findings Genes related to peptide and hormone signaling have been suggested for anxiety-related phenotypes, e.g., the NPSR1 gene, which has been associated predominantly with panic disorder in women, and shown to interact with environmental factors and to influence psychometric, neurophysiological, and neuroimaging correlates of anxiety. Similar multi-level results have been reported for genetic and epigenetic variation in the OXTR gene, especially in social anxiety disorder (SAD), and for CRHR1 gene variation in women with panic disorder. Variants in RGS2 and ASIC1 genes were linked to panic disorder, with the latter also being implicated in SAD treatment response. Finally, monoaminergic ‘risk’ genes (SLC6A4, MAOA, HTR1A) were related to SAD, generalized anxiety disorder and women with panic disorder, anxiety traits and response to psychopharmacological and psychotherapeutic interventions. Summary Converging evidence for potential genetic and epigenetic risk markers has been gathered and future studies call for independent replications and multi-level integration of dimensional approaches, environmental factors, and biological readouts, while considering sex-specific substratification. Particularly, epigenetic variation appears promising for disease course and treatment response predictions.
8
… The finding that the serotonin gene HTR2A SNP rs3742278 is associated with an increase in BAP in the letrozole group is limited by the small sample size but is considered hypothesis-…
9
The article is dedicated to the review of references related to the influence of serotonergic system on the development of autoimmune inflammation. We analysed the data indicating the role of serotonin receptor gene 5-HT2A polymorphism in the development of rheumatic arthritis (RA). We also showed some findings concerning the importance of serotonergic system in regulation of pain syndrome of various origin and demonstrated the significance of gene polymorphism associated with serotonin in regulation of psycho-emotional sphere.
10
Persistent arm pain, a distinct syndrome from persistent breast pain, is a considerable clinical problem following breast cancer surgery. The roles of neurotransmitters and …
11
Only a minority of patients with social anxiety disorder (SAD) has a robust therapeutic response to evidence-based serotonin reuptake inhibitor (SSRI) treatment. To help improve the personalized medicine approach to psychiatric care, we evaluated several candidate genetic predictors of SSRI response in SAD. At the start of a randomized controlled trial (NCT00282828), 346 patients with SAD at three sites received protocol-driven, open-label treatment with sertraline, up to 200. mg/d over 10 weeks. Efficacy was determined using a continuous measure of outcome (Liebowitz Social Anxiety Scale (LSAS)) and dichotomous indicators of response (LSAS ⩽50) and remission (LSAS ⩽30). Predictors of efficacy were examined in multivariate regression models that included eight polymorphic variants in four candidate genes (four in RGS2, two in HTR2A, one in SLC6A2, and one in SLC6A4). Adjusting for genetic ancestral cluster and non-genetic predictors of response, all four single-nucleotide polymorphisms (SNPs) in RGS2 predicted change in LSAS over time, at study-wise significance (p=0.00833), with the minor allele associated with less improvement over time. After adjusting for genetic ancestral cluster and non-genetic predictors of remission, two of the four RGS2 SNPs predicted likelihood of remission at or just below study-wise significance (p=0.025): rs4606 (AOR=0.49 (95% CI=0.27–0.90), p=0.022) and rs1819741 (AOR=0.50 (95% CI=0.28–0.92), p=0.027). Variation in RGS2, a gene previously shown to be associated with social anxiety phenotypes and serotonergic neurotransmission, may be a biomarker of the likelihood of substantially benefiting from sertraline among patients with SAD.
12
We examined the association between 15 single nucleotide polymorphisms (SNPs) in HTR2A and characteristics of disordered eating, including weight/shape concerns, binge eating (with or without loss of control), and compensatory behaviors (purging and nonpurging). Whether a lifetime history of major depressive disorder (MDD) moderated or mediated this association was also investigated. A sample of 1533 twin women of White descent that were part of the Missouri Adolescent Female Twin Study was used. Data were collected using self-report responses to a semistructured interview. Logistic regression analyses were used to examine the association between weight/shape concerns, binge eating, and compensatory behaviors and SNPs (where carriers of the minor allele were coded as 1). Two SNPs, rs6561333 and rs2296972, showed a protective influence against binge eating, with rs2296972 being significant at a trend level after application of the false discovery rate. The SNP was not associated with MDD nor did MDD moderate its putative relation with binge eating. Pending replication, our analyses provide preliminary evidence for intronic SNPs in HTR2A and their association with binge eating. Given the well-documented role of serotonergic dysfunction in eating psychopathology, this report warrants considerable further study.
13
To determine whether single-nucleotide polymorphisms (SNPs) in candidate genes are associated with response to olanzapine-fluoxetine combination. Method: A post hoc …
14
Nardi B, Piva F, Turchi C, Giulietti M, Castellucci G, Arimatea E, Rocchetti D, Rocchetti G, Principato G, Tagliabracci A, Bellantuono C. HTR2A gene polymorphisms and Inward and …
15
This dissertation used a candidate gene study design to determine association of 2345 single nucleotide polymorphisms (SNPs) with neural phenotypes previously linked to …
16
Reciprocity with primary caregivers drives subjects’ adaptive abilities towards the construction of a Personal Meaning Organization (PMO) that is useful with respect to …
17
Anorexia nervosa (AN) is a complex disorder with the highest range of mortality among psychiatric disorders. Genetic studies on twins and families provided from 12 years suggested a …
18
There is evidence for either genetic heterogeneity or complex inheritance with an interaction of environmental factors and multiple single genes in the etiology of panic disorder. …
19
Among the experimentally assessed DNA variations in serotonin related genes, some influence physiological expression of personality and mental disorders, others alter the responses to pharmacological and/or psychotherapeutic treatments. Because of the huge number of polymorphisms lying in genes and of the great length of time necessary to perform association studies, a selection of the variations being studied is a necessary and crucial step.
20
There is mixed evidence of association of serotoninergic genes with anorexia nervosa (AN), but substantial evidence for the involvement of serotonergic mechanisms in appetite control. This study was designed to investigate possible associations between the two subtypes of AN (Restricting-RAN, and Binge-purging–BPAN) and polymorphisms within five genes encoding for proteins involved in the serotoninergic system. Methods. In order to carry out this investigation we have conducted a case–control association study on 226 females meeting the criteria for AN, and 678 matched healthy females. Results. Our data show a significant association between polymorphisms with the gene encoding HTR2A with both AN subtypes, an association between polymorphisms within the genes encoding HTR1D and HTR1B with RAN, and an association between polymorphisms within the gene encoding HTR2C with BPAN. No associations were found for any polymorphisms of the serotonin transporter gene. This outcome indicates a substantial and complex inter-relationship between serotoninergic genes and AN. Conclusions. Given these data we hypothesis that the expression or control of expression of several genes of the serotoninergic system, and interactions between these genes, could exert considerable influence over the specific symptomatology of the subtypes of AN.
21
We have investigated genetic variation in microRNA-mediated regulation as a susceptibility factor for anxiety disorders following two different approaches. We first studied two isoforms …
22
Anxiety disorders and specifically panic disorder (PD) are caused by complex interactions of environmental and genetic factors. The latter comprise many different genes, from which those involved in serotonergic neurotransmission have received particular attention. Here we report the results from an association candidate‐gene approach, where we analyzed 15 single nucleotide polymorphisms (SNPs) within the gene coding for the serotonin‐receptor 2A (HTR2A) in patients suffering from PD and a control sample. We found that the SNP rs2296972 shows an association between the number of T‐alleles and severity of symptoms in PD. By performing tests according to the Fisher product method (FPM), an association between HTR2A and the personality trait reward dependence could be shown. Most pronounced effects were observable for the SNPs rs2770304, rs6313, and rs6311. Furthermore, the polymorphisms rs3742278, rs2296972, and rs2770292 form a haplotype, which may be associated with higher susceptibility for PD. These results further underline a possible important role of genetic variations within the system controlling serotonergic neurotransmission for the development and course of disease in PD. © 2007 Wiley‐Liss, Inc.
23
There is good evidence that panic disorder is a familial disease; however, the extent to which the transmission among family members is genetic has not been resolved. Although there are a number of family studies of anxiety disorders, most have not separated panic from other anxiety disorders, and some use family history, not direct interview methods. Three family studies have included probands with panic disorder and have used direct interviews and specific diagnostic criteria (Cloninger, Martin, Clayton, & Guze, 1981; Crowe, Noyes, Harris, Slymen, & Chaudhry, 1984; Harris, Noyes, Crowe, & Chaudhry, 1983). These studies confirm the highly familial nature of panic disorder. The rates of illness were higher than those reported in the earlier family history studies, but the patterns were similar. The first-degree relatives of probands with panic disorder had markedly elevated rates of panic disorder.
24
Fear in patients with phobic anxiety disorder can be interpreted as a negative bias towards upcoming events: Patients expect specific situations to be bad, threatening, and …
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