G protein gene variants in schizophrenia

Gokce H. H. Y., Daşdemir S., Küçükali C. İ., Iplik E. S., Çakmakoğlu B.

ARCHIVES OF CLINICAL PSYCHIATRY, vol.47, no.2, pp.31-34, 2020 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 47 Issue: 2
  • Publication Date: 2020
  • Doi Number: 10.1590/0101-60830000000227
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, Directory of Open Access Journals
  • Page Numbers: pp.31-34
  • Istanbul University Affiliated: Yes


Background: Various studies demonstrating enhanced vulnerability to apoptosis may contribute to the pathobiology of schizophrenia. Objective: Thus, G proteins may provide an intriguing link between the signal transduction, and apoptotic hypotheses of schizophrenia. In the light of these findings, we investigated whether G protein gene polymorphisms (GNAS1-T393C and GNB3-C825T) accounted for an increased risk of schizophrenia. Methods: The present analyses were based on 100 subjects diagnosed with schizophrenia, and on 100 unrelated healthy controls. The genotyping of GNAS1-T393C. and GNB3-C825T gene polymorphisms were performed using the polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP). Results: We demonstrated the positive association of GNB3-C825T gene variants with schizophrenia risk (p: 0.023). In our study, more prevalent CC genotype frequencies were detected in GNB3 in patients compared with the frequencies in the controls. The individuals with GNB3-C825T CC genotype had 2 fold increased risk for schizophrenia (p: 0.011, chi(2): 6.39, OR:2.14, 95% CI: 1.18-3.90). Discussion: Our study results suggested that GNB3-C825T polymorphism might be associated with schizophrenia.