No evidence for an association between G protein β3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia

Heon Jeong Lee, Seung Gul Kang, Jong Woo Paik, Moon Soo Lee, Bang Hyun Cho, Young Min Park, Won Kim, Jung Eun Choi, In Kwa Jung, Leen Kim, Min Soo Lee

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Objective: Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotic. We evaluated candidate functional polymorphism of the G protein β3 subunit (GNB3) gene for association with drug-induced TD in the Korean schizophrenic patients. Methods: We investigated whether the C825T polymorphism of the GNB3 gene is associated with the TD in a Korean sample of schizophrenic patients with (n = 83) and without TD (n = 126), matched for antipsychotic drug exposure and other relevant variables. Results: The distribution of genotypes and allele frequencies of GNB3 were not different between schizophrenic patients with TD and without TD (p > 0.05). Conclusion: Within the limitations imposed by the size of the clinical sample, these findings suggest that the GNB3 825 C/T single nucleotide polymorphism (SNP) does not contribute significantly to risk for TD.

Original languageEnglish
Pages (from-to)501-504
Number of pages4
JournalHuman Psychopharmacology
Volume22
Issue number8
DOIs
Publication statusPublished - 2007 Dec

Keywords

  • G protein
  • Polymorphism
  • Schizophrenia
  • Tardive dyskinesia

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Pharmacology (medical)

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    Lee, H. J., Kang, S. G., Paik, J. W., Lee, M. S., Cho, B. H., Park, Y. M., Kim, W., Choi, J. E., Jung, I. K., Kim, L., & Lee, M. S. (2007). No evidence for an association between G protein β3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia. Human Psychopharmacology, 22(8), 501-504. https://doi.org/10.1002/hup.875