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Association Study between Serotonin 1A Receptor Gene rs6295 Polymorphism and Tardive Dyskinesia in Patients with Schizophrenia

조현병 환자에서의 지연성 운동이상 발생과 세로토닌 1A 수용체유전자 rs6295 다형성과의 연관성

  • Lee, Youn-Jung (Department of Psychiatry, Gyeongsang National University School of Medicine and Gyeongsang National University Hospital) ;
  • Namgoong, Yoon (Department of Internal Medicine, Korea University Guro Hospital) ;
  • Cho, Areum (Department of Psychiatry, Korea University College of Medicine) ;
  • Lee, Heon-Jeong (Department of Psychiatry, Korea University College of Medicine)
  • 이윤정 (경상대학교병원 정신건강의학과학교실) ;
  • 남궁윤 (고려대학교구로병원 내과) ;
  • 조아름 (고려대학교 의과대학 정신건강의학교실) ;
  • 이헌정 (고려대학교 의과대학 정신건강의학교실)
  • Received : 2020.06.26
  • Accepted : 2020.09.24
  • Published : 2020.10.30

Abstract

Objectives: Tardive dyskinesia (TD) is a movement disorder that is characterized by hyperkinetic movements. Previous studies have suggested that the serotonergic systems are correlated with TD vulnerability. In this study, the association between a single-nucleotide polymorphism (SNP) of the serotonin 1A receptor gene (HTR1A) rs6295 and TD was investigated. Methods: We investigated whether HTR1A rs6295 SNP is associated with antipsychotic-induced TD in 280 Korean patients with schizophrenia. Patients with schizophrenia having TD (n=105) and those without TD (n=175) were matched for their antipsychotic exposures and other relevant variables. The HTR1A rs6295 SNP was analyzed using polymerase chain reaction (PCR)-based methods. Results: There was no significant difference in the distribution of genotypic (χ2=2.70, p=0.26) and allelic (χ2=1.87, p=0.17) frequencies between the patient groups with TD and without TD. There was no significant difference in total abnormal involuntary movement scale score (F=0.39, p=0.68) among the genotype group either. Conclusion: Although there were no differences in genotypic and allelic frequency between patient groups with and without TD, further studies on association of TD with other SNPs of HTRA1 are needed to understand the pathophysiological mechanism of TD.

Keywords

References

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