The PTPRD (Protein Tyrosine Phosphatase Receptor Type Delta) Gene Polymorphism and Antipsychotic-Induced Restless Legs Syndrome in Schizophrenia.
10.16946/kjsr.2014.17.1.43
- Author:
Ho Jin JUNG
;
Chul Hyun CHO
;
Seung Gul KANG
;
Heon Jeong LEE
- Publication Type:Original Article
- Keywords:
Restless legs syndrome;
PTPRD;
Schizophrenia
- MeSH:
Gene Frequency;
Genetic Predisposition to Disease;
Genome-Wide Association Study;
Genotype;
Humans;
Polymerase Chain Reaction;
Restless Legs Syndrome*;
Schizophrenia*;
Tyrosine*
- From:Korean Journal of Schizophrenia Research
2014;17(1):43-46
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: The previous genome-wide association studies have revealed several candidate genes for restless legs syndrome (RLS). The PTPRD (protein tyrosine phosphatase receptor type delta) gene is one of the candidate genes for RLS. The occurrence of antipsychotic-related RLS could also be attributable to differences in genetic susceptibility. This study aimed to investigate whether PTPRD polymorphism is associated with antipsychotic-related RLS in schizophrenia. METHODS: We assessed symptoms of antipsychotic-induced RLS in 190 Korean schizophrenic patients and divided the subjects into two groups according to the International Restless Legs Syndrome Study Group diagnostic criteria : (i) subjects that met all of the criteria (n=44) and (ii) the remaining subjects who were not considered to be RLS patients (n=146). PTPRD rs462664 was genotyped by PCR in 190 individuals. The chi2-test was performed to compare differences between two groups. RESULTS: The frequencies of genotype (chi2=1.31, p=0.519) of the PTPRD rs462664 did not differ significantly between schizophrenic patients with and without RLS. The difference of allele frequencies (chi2=1.30, p=0.25) of the PTPRD rs462664 between the schizophrenic patients with and without RLS were not significant. CONCLUSION: These results suggest that PTPRD gene polymorphism does not play a major role in susceptibility to antipsychotic-related RLS in schizophrenia. This finding suggests that antipsychotic-induced RLS may have a different pathogenesis compared to primary RLS.
