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ID 32940
フルテキストURL
著者
Uchida, Naohiko Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Ujike, Hiroshi Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Nakata, Kenji Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Takaki, Manabu Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Nomura, Akira Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Katsu, Takeshi Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Tanaka, Yuji Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Imamura, Takaki Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Sakai, Ayumu Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
Kuroda, Shigetoshi Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
抄録

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.
Conclusion: In view of this evidence, it is likely that the SIGMAR1 gene does not confersusceptibility to schizophrenia.

備考
Digital Object Identifier: 10.1186/1471-244X-3-13
Published with permission from the copyright holder. This is the institute's copy, as published in BMC Psychiatry, 21 October 2003, 3:13.
Publisher URL:http://dx.doi.org/10.1186/1471-244X-3-13
Copyright © 2003 Uchida et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
発行日
2003-10-21
出版物タイトル
BMC Psychiatry
3巻
出版者
BioMed Central
NCID
AA12072671
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
著作権者
Uchida et al; licensee BioMed Central Ltd.
論文のバージョン
publisher
査読
有り
DOI
PubMed ID
Submission Path
internal_medicine/3