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      SCIE SSCI SCOPUS KCI등재

      The Association between the T102C Polymorphism of Serotonin-2A Receptor Gene and Neurocognitive Function in Obsessive Compulsive Disorder

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      https://www.riss.kr/link?id=A105324696

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      다국어 초록 (Multilingual Abstract)

      Serotonin dysfunction has been implicated in the pathogenesis of obsessive compulsive disorder (OCD). Neurocognitive dysfunction is considered as the core pathology in the OCD. This study aimed to investigate the association of T102C polymorphism of t...

      Serotonin dysfunction has been implicated in the pathogenesis of obsessive compulsive disorder (OCD). Neurocognitive dysfunction is considered as the core pathology in the OCD. This study aimed to investigate the association of T102C polymorphism of the 5-HT2A receptor gene with the neurocognitive function in OCD. Fifty four patients with OCD were participated in this study. Neurocognitive function tests were administered to the patients with OCD. T102C of the 5-HT2A gene were analyzed by Polymerase Chain Reaction (PCR) amplification and Restriction Fragment Length Polymorphism (RFLP). The distribution of genotypic patterns of T102C was grouped into T/T genotype (n=16), T/C genotype (n=28) and T/T genotype (n=10). The group of patients with T/T genotype demonstrated significant delayed response time in immediate recall (p=0.036) and delayed recall (p=0.038) of Rey-Osterrieth Complex Figure test which was used to evaluate visuospatial construction ability and visuospatial memory. These results showed that T/T genotype of T102C has higher performance deficit in neurocognitive function tests such as RCFT than the other types. We suggest that T102C genotype may contribute to neurocognitive function and neurocognitive function may serve as a good candidate phenotype for association or linkage studies on OCD.

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      목차 (Table of Contents)

      • INTRODUCTION
      • METHODS
      • RESULTS
      • DISCUSSION
      • ACKNOWLEDGEMENTS
      • INTRODUCTION
      • METHODS
      • RESULTS
      • DISCUSSION
      • ACKNOWLEDGEMENTS
      • References
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