This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of the proposed research is to study the neurobiology and treatment of social anxiety disorder (SAD). Although approximately half of patients with SAD fail to respond to first-line selective serotonin reuptake inhibitor (SSRI) treatment despite adequate dose and duration, little is known about the neurophysiological mechanisms underlying treatment efficacy. Converging evidence suggests that amygdala reactivity to social threat and a functional polymorphism on the sertonin transporter gene (5-HTTLPR) are potential biomarkers of SSRI treatment response. The proposed research focuses on elucidating the neuro-genetic basis of pharmacologic treatment response in SAD through the application of brain functional magnetic resonance imaging (fMRI) and pharmacogenetics. In the context of an open-label clinical trial of sertraline, this study proposes to perform pre- and post-treatment fMRI of amygdala reactivity to harsh/negative face/social stimuli and pre-treatment DNA genotyping of the 5-HTTLPR in 80 patients with generalized SAD and 80 matched healthy controls in order to examine the relationship between these neuro-genetic markers and treatment response. Our hypotheses regarding the 5-HTTLPR, for which we request CRC support are: Hypothesis 1: SAD patients with the homozygous long allele genotype (L/L) will have greater anti-anxiety response to sertraline, compared to those with the S/S genotype. Hypothesis 2: Genotypic variation of the 5-HTTLPR will predict response to treatment, such that the S/S genotype will be associated with a higher likelihood of non-response to treatment, relative to the L/L genotype.
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