Association study of GRIK1 gene polymorphisms in schizophrenia: Case-control and family-based studies

Yuko Hirata, Clement C. Zai, Renan P. Souza, Jeffrey A. Lieberman, Herbert Y. Meltzer, James L. Kennedy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Glutamatergic function is one of the major hypotheses for schizophrenia. Within the glutamate system, the glutamate receptor ionotropic kainate-1 (GRIK1) gene is thought to be particularly involved in schizophrenia because of the reported reduction of GRIK1 in the dorsolateral prefrontal cortex of patients. Objective We examined single-nucleotide polymorphisms (SNPs) in the GRIK1 gene for possible association with schizophrenia. Methods We analyzed eight SNPs across the GRIK1 gene in 202 case-control pairs and 108 small nuclear families. Results For the case-control study, we found nominal significant associations in the analysis of rs469472 (p = 0.028) and its haplotypes. In the family-based study, nominal significant association was also observed for rs469472 (p = 0.046), as well as rs455892 (p = 0.024). The marker rs469472 was associated with schizophrenia when we combined the case-control and family samples (p = 0.027). The association findings did not survive correction for multiple testing. Conclusions Because we observed similar association findings with marker rs469472 in two independent samples, further analyses in larger samples are warranted.

Original languageEnglish (US)
Pages (from-to)345-351
Number of pages7
JournalHuman Psychopharmacology
Issue number4
StatePublished - Jul 2012


  • GluR5 glutamate receptor ionotropic kainate-1 gene (GRIK1)
  • case-control
  • family-based association study
  • genetics
  • schizophrenia

ASJC Scopus subject areas

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


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