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Background: Tardive dyskinesia (TD) is an extrapyramidal side effect of the long-term use of antipsychotics. In the present study, the role of glutamatergic system genes in the pathogenesis of total TD, as well as two phenotypic forms, orofacial TD and limb-truncal TD, was studied. Methods: A set of 46 SNPs of the glutamatergic system genes (<i>GRIN2A</i>, <i>GRIN2B</i>, <i>GRIK4</i>, <i>GRM3</i>, <i>GRM7</i>, <i>GRM8</i>, <i>SLC1A2</i>, <i>SLC1A3</i>, <i>SLC17A7</i>) was studied in a population of 704 Caucasian patients with schizophrenia. Genotyping was performed using the MassARRAY Analyzer 4 (Agena Bioscience™). Logistic regression analysis was performed to test for the association of TD with the SNPs while adjusting for confounders. Results: No statistically significant associations between the SNPs and TD were found after adjusting for multiple testing. Since three SNPs of the <i>SLC1A2</i> gene demonstrated nominally significant associations, we carried out a haplotype analysis for these SNPs. This analysis identified a risk haplotype for TD comprising CAT alleles of the <i>SLC1A2</i> gene SNPs rs1042113, rs10768121, and rs12361171. Nominally significant associations were identified for <i>SLC1A3</i> rs2229894 and orofacial TD, as well as for <i>GRIN2A</i> rs7192557 and limb-truncal TD. Conclusions: Genes encoding for mGlu3, EAAT2, and EAAT1 may be involved in the development of TD in schizophrenia patients.