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ID 32940
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Author
Uchida, Naohiko
Ujike, Hiroshi
Nakata, Kenji
Nomura, Akira
Katsu, Takeshi
Tanaka, Yuji
Imamura, Takaki
Sakai, Ayumu
Kuroda, Shigetoshi
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.
Conclusion: In view of this evidence, it is likely that the SIGMAR1 gene does not confersusceptibility to schizophrenia.

Note
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.
Published Date
2003-10-21
Publication Title
BMC Psychiatry
Volume
volume3
Publisher
BioMed Central
NCID
AA12072671
Content Type
Journal Article
language
英語
Copyright Holders
Uchida et al; licensee BioMed Central Ltd.
File Version
publisher
Refereed
True
DOI
PubMed ID
Submission Path
internal_medicine/3