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Association of the serotonin transporter promoter region polymorphism with biased attention for negative word stimuli.

ABSTRACT: BACKGROUND:Biased attention for emotional stimuli reflects vulnerability or resilience to emotional disorders. The current study examines whether the 5-HTTLPR polymorphism is associated with attentional biases for negative word stimuli. METHODS:Unmedicated, young adults with low current depression and anxiety symptoms (N=106) were genotyped for the 5-HTTLPR, including the single nucleotide polymorphism (SNP) rs25531 in the long allele of the 5-HTTLPR. Participants then completed a standard dot-probe task that measured attentional bias toward anxiety, dysphoric, and self-esteem words. RESULTS:The L(A)L(A) allele group demonstrated an attentional bias away from negative word stimuli. This attentional bias was absent among the S/L(G) carriers. CONCLUSIONS:These findings replicate previous work and suggest that 5-HTTLPR L(A) homozygotes possess a protective attentional bias that may decrease susceptibility to depression and anxiety.

SUBMITTER: Kwang T

PROVIDER: S-EPMC2919243 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Association of the serotonin transporter promoter region polymorphism with biased attention for negative word stimuli.

Kwang Tracy T Wells Tony T TT McGeary John E JE Swann William B WB Beevers Christopher G CG

Depression and anxiety 20100801 8

<h4>Background</h4>Biased attention for emotional stimuli reflects vulnerability or resilience to emotional disorders. The current study examines whether the 5-HTTLPR polymorphism is associated with attentional biases for negative word stimuli.<h4>Methods</h4>Unmedicated, young adults with low current depression and anxiety symptoms (N=106) were genotyped for the 5-HTTLPR, including the single nucleotide polymorphism (SNP) rs25531 in the long allele of the 5-HTTLPR. Participants then completed a ...[more]

PMID: 20694965

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Project description:Panic disorder (PD) and social anxiety disorder (SAD) are moderately heritable anxiety disorders. We analyzed five genes, derived from pharmacological or translational mouse models, in a new case-control study of PD and SAD in European Americans: (1) the serotonin transporter (SLC6A4), (2) the serotonin receptor 1A, (3) catechol-O-methyltransferase, (4) a regulator of g-protein signaling and (5) the gastrin-releasing peptide receptor. Cases were interviewed using the schedule for affective disorders and schizophrenia and were required to have a probable or definite lifetime diagnosis of PD (N=179), SAD (161) or both (140), with first onset by age 31 and a family history of anxiety. Final diagnoses were determined using the best estimate procedure, blind to genotyping data. Controls were obtained from the National Institute of Mental Health Human Genetics Initiative; only subjects above 25 years of age who screened negative for all psychiatric symptoms were included (N=470). A total of 45 single nucleotide polymorphisms were successfully genotyped over the five selected genes using Applied Biosystems SNPlex protocol. SLC6A4 provided strong and consistent evidence of association with the PD and PD+SAD groups, with the most significant association in both groups being at rs140701 (chi(2)=10.72, P=0.001 with PD and chi(2)=8.59, P=0.003 in the PD+SAD group). This association remained significant after multiple test correction. Those carrying at least one copy of the haplotype A-A-G constructed from rs3794808, rs140701 and rs4583306 have 1.7 times the odds of PD than those without the haplotype (95% confidence interval: 1.2-2.3). The SAD only group did not provide evidence of association, suggesting a PD-driven association. The findings remained after adjustment for age and sex, and there was no evidence that the association was due to population stratification. The promoter region of the gene, 5-HTTLPR, did not provide any evidence of association, regardless of whether analyzed as a triallelic or biallelic locus, nor did any of the other four candidate genes tested. Our findings suggest that the serotonin transporter gene may play a role in PD; however, the findings require replication. Future studies should attend to the entire genetic region rather than the promoter.

Dataset Information

Association of the serotonin transporter promoter region polymorphism with biased attention for negative word stimuli.

Publications

Association of the serotonin transporter promoter region polymorphism with biased attention for negative word stimuli.

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