Possible association between Interleukin-1beta gene and schizophrenia in a Japanese population
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RESEARCH
Open Access
Possible association between Interleukin-1beta gene and schizophrenia in a Japanese population Daimei Sasayama1,2*, Hiroaki Hori1,3, Toshiya Teraishi1, Kotaro Hattori1, Miho Ota1, Yoshimi Iijima4, Masahiko Tatsumi5, Teruhiko Higuchi6, Naoji Amano2 and Hiroshi Kunugi1,3
Abstract Background: Several lines of evidence have implicated the pro-inflammatory cytokine interleukin-1beta (IL-1b) 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-1b 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-1b gene polymorphism rs1143633 is associated with schizophrenia susceptibility in a Japanese population. The results suggest the possibility that the influence of IL-1b 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-1b in the etiology of schizophrenia.
Background Several lines of evidence suggest that pro-inflammatory cytokine interleukin-1beta (IL-1b) is implicated in the etiology and pathophysiology of schizophrenia. Although studies investigating peripheral levels of IL-1b in schizophrenic patients have reported inconsistent results [1-6], a study examining the cerebrospinal fluid has shown a marked elevation of IL-1b in patients with first-episode schizophrenia compared to healthy controls [7]. Kowalski et al [8] reported that the release of IL-1b by peripheral monocytes was increased before treatment and then normalized by antipsychotic medication in patients with schizophrenia. Recently, Liu et al. [9] showed that IL-1b in the peripheral blood mononuclear cells was overexpressed not * Correspondence: [email protected] 1 Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, 187-8502, Japan Full list of author information is available at the end of the article
only in schizophrenia patients but also in their siblings, suggesting the involvement of the
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