Behavioral and Brain Functions (Aug 2011)

Possible association between <it>Interleukin-1beta </it>gene and schizophrenia in a Japanese population

  • Sasayama Daimei,
  • Hori Hiroaki,
  • Teraishi Toshiya,
  • Hattori Kotaro,
  • Ota Miho,
  • Iijima Yoshimi,
  • Tatsumi Masahiko,
  • Higuchi Teruhiko,
  • Amano Naoji,
  • Kunugi Hiroshi

DOI
https://doi.org/10.1186/1744-9081-7-35
Journal volume & issue
Vol. 7, no. 1
p. 35

Abstract

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Abstract Background Several lines of evidence have implicated the pro-inflammatory cytokine interleukin-1beta (IL-1β) in the etiology of schizophrenia. Although a number of genetic association studies have been reported, very few have systematically examined gene-wide tagging polymorphisms. Methods A total of 533 patients with schizophrenia (302 males: mean age ± standard deviation 43.4 ± 13.0 years; 233 females; mean age 44.8 ± 15.3 years) and 1136 healthy controls (388 males: mean age 44.6 ± 17.3 years; 748 females; 46.3 ± 15.6 years) were recruited for this study. All subjects were biologically unrelated Japanese individuals. Five tagging polymorphisms of IL-1β gene (rs2853550, rs1143634, rs1143633, rs1143630, rs16944) were examined for association with schizophrenia. Results Significant difference in allele distribution was found between patients with schizophrenia and controls for rs1143633 (P = 0.0089). When the analysis was performed separately in each gender, significant difference between patients and controls in allele distribution of rs1143633 was observed in females (P = 0.0073). A trend towards association was also found between rs16944 and female patients with schizophrenia (P = 0.032). Conclusions The present study shows the first evidence that the IL-1β gene polymorphism rs1143633 is associated with schizophrenia susceptibility in a Japanese population. The results suggest the possibility that the influence of IL-1β gene variations on susceptibility to schizophrenia may be greater in females than in males. Findings of the present study provide further support for the role of IL-1β in the etiology of schizophrenia.