Genetic study of eight AKT1 gene polymorphisms and their interaction with DRD2 gene polymorphisms in tardive dyskinesia

Clement C. Zai, Marco A. Romano-Silva, Rudi Hwang, Gwyneth C. Zai, Vincenzo DeLuca, Daniel J. Müller, Nicole King, Aristotle N. Voineskos, Herbert Y. Meltzer, Jeffrey A. Lieberman, Steven G. Potkin, Gary Remington, James L. Kennedy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Tardive dyskinesia (TD) is a motor adverse effect of chronic antipsychotic medication. It has been suggested to involve dopamine neurotransmission system changes. AKT1 acts downstream of the D2 receptor that is blocked by all antipsychotics to some degree. The AKT1 gene has not been investigated in TD. We examined eight polymorphisms spanning the AKT1 gene and their association with TD in our schizophrenia sample of 193 Caucasians, 76 of which with TD. AKT1 polymorphisms and haplotypes were not significantly associated with TD. However, we detected a significant interaction between rs6275 of DRD2 and rs3730358 of AKT1 (p < 1 × 10- 5).

Original languageEnglish (US)
Pages (from-to)248-252
Number of pages5
JournalSchizophrenia Research
Volume106
Issue number2-3
DOIs
StatePublished - Dec 1 2008

Keywords

  • Dopamine receptor DRD2 gene
  • Gene association
  • Genetic interaction
  • Protein kinase B PKB/AKT1
  • Schizophrenia
  • Tardive dyskinesia

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry

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