Gene polymorphisms of glutamatergic system in drug-induced dyskinesias in patients with schizophrenia and Parkinson's disease

Pathogenesis of the development of drug-induced disorders against the background of the use of antipsychotics and antiparkinsonian agents is not sufficiently studied. At present, studies of glutamatergic system and its role in the development of dyskinesias are widely prevalent in the literature. Objective of the work is to study polymorphic variants of genes of NMDA-receptor and glutamate transporter SLC1A2 in drug-induced dyskinesias in patients with schizophrenia and Parkinson's disease. A complex clinical biological examination of 180 patients with schizophrenia and 187 patients with Parkinson's disease is carried out. Associations of polymorphism of gene SLC1A2 with the development of tardive dyskinesia in patients with schizophrenia and polymorphism rs2650427 of the gene GRIN2A with the development of levodopa-induced dyskinesia in Parkinson's disease are revealed. Regarding polymorphism rs1969060 of the gene GRIN2A, a decrease in the incidence rate of the genotype GG in schizophrenic patients with tardive dyskinesia in comparison with the indices of patients without tardive dyskinesia is observed whereas in patients with levodopa-induced dyskinesia increase in the incidence rate of the genotype GG is revealed that can give evidence of different pharmacogenetic features of the development of dyskinesias in different pathologies. Findings of research show that polymorphic features of genes of glutamatergic system are an important link of the pathogenesis of extrapyramidal side effects observed against the background of antipsychotic therapy in patients with schizophrenia and use of levodopa in Parkinson's disease patients.