PMID- 31118638 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20201001 IS - 1176-6328 (Print) IS - 1178-2021 (Electronic) IS - 1176-6328 (Linking) VI - 15 DP - 2019 TI - Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population. PG - 989-1000 LID - 10.2147/NDT.S194924 [doi] AB - Background: Excitatory amino acid transporter 2 encoded by SLC1A2 is responsible for approximately 90% of glutamate uptake. Glycine transporter 1, encoded by SLC6A9, is responsible for maintaining a low concentration of the N-methyl-D-aspartate receptor (NMDAR) co-agonist - glycine in the synaptic cleft, suggesting its participation in the development of the NMDARs hypofunction described in schizophrenia. Aim: The aim of this study was to evaluate whether the functional polymorphism-181 A/C (rs4354668) of the SLC1A2 and the rs2486001 (IVS3+411 G/A) in the SLC6A9 are involved in schizophrenia development and its clinical picture in the Polish population. Methods: The study group consisted of 393 unrelated Caucasian patients (157 [39.9%] females and 236 [60.1%] males; mean age 41+/-12) diagnosed with schizophrenia according to the DSM-5, and 462 healthy controls. The results of the Positive and Negative Syndrome Scale (PANSS) were presented in the five-dimensional model. Polymorphisms of SLC1A2 and SLC6A9 were genotyped with the use of PCR-RFLP assay. Results: There were no statistically significant differences in the frequency of genotypes and alleles between the patients and controls for SLC1A2 and SLC6A9 polymorphisms in either the entire sample or after stratification according to gender. In the haplotype analysis, men with CA haplotype had more than 1.5 higher risk to develop schizophrenia than women (OR=1.63 [95% CI=1.17-2.27, p<0.05]). The influence of gender, genotypes of both analyzed polymorphisms and gender x genotype interactions on individual dimensions of the PANSS scale has not been observed. Also, there was no association of either polymorphism with suicide attempts. Conclusion: The results of the present study did not indicate an association of polymorphism-181 A/C (rs4354668) in SLC1A2 and rs2486001 in SLC6A9 with onset of schizophrenia and its psychopathology in a Polish population. FAU - Merk, Wojciech AU - Merk W AUID- ORCID: 0000-0001-7080-1063 AD - Department of Psychiatry and Psychotherapy, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland. FAU - Kucia, Krzysztof AU - Kucia K AUID- ORCID: 0000-0001-5618-2833 AD - Department of Psychiatry and Psychotherapy, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland. FAU - Medrala, Tomasz AU - Medrala T AUID- ORCID: 0000-0001-6880-6471 AD - Department of Psychiatry and Psychotherapy, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland. FAU - Kowalczyk, Malgorzata AU - Kowalczyk M AD - Department of Medical Genetics, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland. FAU - Owczarek, Aleksander AU - Owczarek A AD - Division of Statistics, Department of Instrumental Analysis, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland. AD - Department of Instrumental Analysis, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland. FAU - Kowalski, Jan AU - Kowalski J AD - Department of Medical Genetics, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Poland. LA - eng PT - Journal Article DEP - 20190424 PL - New Zealand TA - Neuropsychiatr Dis Treat JT - Neuropsychiatric disease and treatment JID - 101240304 PMC - PMC6499478 OTO - NOTNLM OT - PANSS OT - excitatory amino acid transporter 2 OT - glutamate system OT - glycine transporter 1 OT - polymorphism OT - schizophrenia COIS- The authors report no conflicts of interest in this work. EDAT- 2019/05/24 06:00 MHDA- 2019/05/24 06:01 PMCR- 2019/04/24 CRDT- 2019/05/24 06:00 PHST- 2018/11/16 00:00 [received] PHST- 2019/02/14 00:00 [accepted] PHST- 2019/05/24 06:00 [entrez] PHST- 2019/05/24 06:00 [pubmed] PHST- 2019/05/24 06:01 [medline] PHST- 2019/04/24 00:00 [pmc-release] AID - 194924 [pii] AID - 10.2147/NDT.S194924 [doi] PST - epublish SO - Neuropsychiatr Dis Treat. 2019 Apr 24;15:989-1000. doi: 10.2147/NDT.S194924. eCollection 2019.