Lack of Association between Brain-Derived Neurotrophic Factor Gene Val66Met Polymorphisms and Generalized Social Anxiety Disorder in Korean Population
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Objective: Several lines of evidence suggest that brain-derived neurotrophic factor (BDNF) plays a role in the pathophysiology of anxiety. We analyzed the association of the BDNF gene polymorphism, G196A (val66met), in the coding region of exon XIIIA in chromosome 11p13, and generalized social anxiety disorder (GSAD). Methods: Patients with GSAD (n=73) and age-matched control subjects (n=152) were tested for the BDNF (val66met)polymorphism. A clinical interview and a Mini-International Neuropsychiatric Interview were conducted by trained psychiatrists in order to diagnose GSAD. The symptomatic characteristics of the GSAD patients were assessed with the Hamilton Anxiety Rating Scale, the Beck Anxiety Inventory, the Retrospective Self Report of Inhibition, the Spielberger State-Trait Anxiety Inventory,and the Liebowitz Social Anxiety Scale. Results: There were no significant differences in the frequencies of the genotypes (χ^2=0.961, degree of freedom [df]=2, p=0.619),alleles (χ^2=0.415, df=1, p=0.519), or allele (methionine) carriers (χ^2=0.019, df=1, p=0.889) between the patients and controls. In addition, when we compared the severity of social anxiety symptom as determined by the clinical scales with the genotypes of the BDNF gene, we could not find any significant differences between the genotypes or allele carriers. Conclusion: These results do not support the hypothesis that the BDNF gene might be a candidate gene for susceptibility or severity of GSAD in the Korean population in this study.
Abstract
Objective: Several lines of evidence suggest that brain-derived neurotrophic factor (BDNF) plays a role in the pathophysiology of anxiety. We analyzed the association of the BDNF gene polymorphism, G196A (val66met), in the coding region of exon XIIIA in chromosome 11p13, and generalized social anxiety disorder (GSAD). Methods: Patients with GSAD (n=73) and age-matched control subjects (n=152) were tested for the BDNF (val66met)polymorphism. A clinical interview and a Mini-International Neuropsychiatric Interview were conducted by trained psychiatrists in order to diagnose GSAD. The symptomatic characteristics of the GSAD patients were assessed with the Hamilton Anxiety Rating Scale, the Beck Anxiety Inventory, the Retrospective Self Report of Inhibition, the Spielberger State-Trait Anxiety Inventory,and the Liebowitz Social Anxiety Scale. Results: There were no significant differences in the frequencies of the genotypes (χ^2=0.961, degree of freedom [df]=2, p=0.619),alleles (χ^2=0.415, df=1, p=0.519), or allele (methionine) carriers (χ^2=0.019, df=1, p=0.889) between the patients and controls. In addition, when we compared the severity of social anxiety symptom as determined by the clinical scales with the genotypes of the BDNF gene, we could not find any significant differences between the genotypes or allele carriers. Conclusion: These results do not support the hypothesis that the BDNF gene might be a candidate gene for susceptibility or severity of GSAD in the Korean population in this study.
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