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Schizophrenia Bulletin Advance Access originally published online on February 9, 2006
Schizophrenia Bulletin 2006 32(2):203-208; doi:10.1093/schbul/sbj058
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© The Author 2006. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Can RGS4 Polymorphisms Be Viewed as Credible Risk Factors for Schizophrenia? A Critical Review of the Evidence

Michael E Talkowski2,3,, KV Chowdari2, David A Lewis2,4, and Vishwajit L Nimgaonkar1,2,3,
2 Department of Psychiatry, University of Pittsburgh School of Medicine
3 Department of Human Genetics, University of Pittsburgh Graduate School of Public Health
4 Department of Neuroscience, University of Pittsburgh School of Medicine

1To whom correspondence should be addressed; Departments of Psychiatry and Human Genetics, University of Pittsburgh School of Medicine, and Graduate School of Public Health, Western Psychiatric Institute and Clinic, Room 441, 3811 O'Hara St., Pittsburgh, PA 15213; tel.: 412-246-6353, fax: 412-246-6350; e-mail: nimga{at}pitt.edu.

There has been a recent explosion in the list of putative susceptibility genes for schizophrenia (SZ). These genes have been identified on the basis of presumed pathogenesis, linkage, and genetic association studies. While several promising candidates have arisen, identification of a conclusive genetic risk factor has remained elusive. The proof would be most compelling if it stemmed from all three of these domains. In this review, we consider such evidence in relation to the regulator of G-protein signaling 4 (RGS4), a gene localized to chromosome 1q23. Disorder-specific changes in RGS4 mRNA levels have been observed in post-mortem brain samples; linkage has been reported at chromosome 1q23; and several association studies have concluded that significant associations exist. The latter are supported by a recently conducted meta-analysis. Thus, there is suggestive evidence in each of these domains implicating a role for RGS4 in SZ susceptibility. However, analogous to other promising susceptibility candidates, the nature of the genetic association, the precise polymorphism(s) conferring risk, and the functional implications of sequence variation at this gene are unclear. We review the published data and place them in the context of suggested criteria for establishing a candidate gene as a credible susceptibility factor for disorders with non-Mendelian patterns of inheritance.

Keywords: schizophrenia / genetic risk / RGS4 / polymorphisms / association / linkage


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