Journal
PSYCHOPHARMACOLOGY
Volume 200, Issue 2, Pages 177-186Publisher
SPRINGER
DOI: 10.1007/s00213-008-1193-9
Keywords
schizophrenia; clozapine response; GSK3 beta; Wnt signaling; genetic association; family-based association test
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Funding
- CNPq-Brazil [202447/2006-5, 140950/2005-2, 554496/2005-4]
- National Institutes of Health (NIH)
- Canadian Institutes of Health Research (CIHR) [940595]
- Ontario Mental Health Foundation (OMHF)
- Fapemig-Brazil
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Rationale A number of human and animal studies implicate GSK3 in the pathophysiology and genetics of schizophrenia. In general, the data suggest that phosphorylation levels of GSK3 beta are reduced in schizophrenia, resulting in increased GSK3 beta activity. Since GSK3 beta regulation is altered in schizophrenia, polymorphic variation in this gene may affect susceptibility to schizophrenia or treatment response. Objective To analyze GSK3 beta genetic variants for association with schizophrenia and clozapine response. Materials and methods We examined GSK3 beta markers in 185 matched case-control subjects, 85 small nuclear families, and 150 schizophrenia patients treated with clozapine for 6 months. Results Three markers (rs7624540, rs4072520, and rs6779828) showed genotypic association with schizophrenia in the case-control sample. We did not observe any family and clozapine response association with a specific allele, genotype, or haplotype. Conclusions Our results suggest that GSK3 beta polymorphisms might be involved in schizophrenia risk but do not appear to play a significant role in clozapine response.
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