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Abstract：
BACKGROUND: Several lines of evidence have supported possible roles of the sigma receptors in the etiology of schizophrenia and mechanisms of antipsychotic efficacy. An association study provided genetic evidence that the sigma receptor type 1 gene (SIGMAR1) was a possible susceptibility factor for schizophrenia, however, it was not replicated by a subsequent study. It is necessary to evaluate further the possibility that the SIGMAR1 gene is associated with susceptibility to schizophrenia.
METHODS: A case-control association study between two polymorphisms of the SIGMAR1 gene, G-241T/C-240T and Gln2Pro, and schizophrenia in Japanese population, and meta-analysis including present and previous studies.
RESULTS: There was no significant association of any allele or genotype of the polymorphisms with schizophrenia. Neither significant association was observed with hebephrenic or paranoid subtype of schizophrenia. Furthermore, a meta-analysis including the present and previous studies comprising 779 controls and 636 schizophrenics also revealed no significant association between the SIGMAR1 gene and schizophrenia.
CONCLUSIONS: In view of this evidence, it is likely that the SIGMAR1 gene does not confer susceptibility to schizophrenia.
METHODS: A case-control association study between two polymorphisms of the SIGMAR1 gene, G-241T/C-240T and Gln2Pro, and schizophrenia in Japanese population, and meta-analysis including present and previous studies.
RESULTS: There was no significant association of any allele or genotype of the polymorphisms with schizophrenia. Neither significant association was observed with hebephrenic or paranoid subtype of schizophrenia. Furthermore, a meta-analysis including the present and previous studies comprising 779 controls and 636 schizophrenics also revealed no significant association between the SIGMAR1 gene and schizophrenia.
CONCLUSIONS: In view of this evidence, it is likely that the SIGMAR1 gene does not confer susceptibility to schizophrenia.
摘要：
背景：一些证据支持σ受体在精神分裂症的病因和抗精神病药效机制中的可能作用。一项关联研究提供了遗传学证据，表明sigma受体1型基因（SIGMAR1）是精神分裂症的可能易感因素，然而,随后的研究未将其复制.有必要进一步评估SIGMAR1基因与精神分裂症易感性相关的可能性。
方法：SIGMAR1基因两个多态性之间的病例对照关联研究，G-241T/C-240T和Gln2Pro，和精神分裂症在日本人群中，和荟萃分析，包括目前和以前的研究。
结果：多态性的任何等位基因或基因型与精神分裂症均无显著关联。与精神分裂症的hebeprenic或偏执亚型均未观察到显着关联。此外，一项荟萃分析,包括本研究和以前的研究,包括779名对照和636名精神分裂症患者,也显示SIGMAR1基因与精神分裂症之间没有显著关联.
结论：鉴于这一证据，SIGMAR1基因可能不赋予精神分裂症易感性.
方法：SIGMAR1基因两个多态性之间的病例对照关联研究，G-241T/C-240T和Gln2Pro，和精神分裂症在日本人群中，和荟萃分析，包括目前和以前的研究。
结果：多态性的任何等位基因或基因型与精神分裂症均无显著关联。与精神分裂症的hebeprenic或偏执亚型均未观察到显着关联。此外，一项荟萃分析,包括本研究和以前的研究,包括779名对照和636名精神分裂症患者,也显示SIGMAR1基因与精神分裂症之间没有显著关联.
结论：鉴于这一证据，SIGMAR1基因可能不赋予精神分裂症易感性.
