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Association of GSK-3β −50T/C Polymorphism with Depression and Cognitive Impairment in Patients with Schizophrenia

박성우|김영훈|이정구|Min Chul Kim|Sun Jung Lee|Sung Soo Jung
대한정신약물학회 (Korean College of Neuropsychopharmacology)|2010.12|Clinical Psychopharmacology and Neuroscience|제8권 제3호|pp. 137-143

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키워드

CognitionDepressionSchizophreniaGlycogen synthase kinase-3βPolymorphism.

초록

Objective: In this study, authors wanted to find out the association between the glycogen synthase kinase-3β (GSK-3β) −50T/C polymorphism and depression and cognitive impairment in patients with schizophrenia. 207 schizophrenia and 100 normal subjects were participated. We evaluated Brief Psychiatric Rating Scale (BPRS), the Hamilton Depression Rating Scale (HAM-D), and the Korean version of the Mini Mental Status Examination (K-MMSE) in schizophrenia. Methods: Polymerase chain reaction (PCR) analysis of genomic DNA was conducted to evaluate the genotype distribution and allele frequency of GSK-3β −50T/C in subjects. Results: We observed that genotype distribution and allele frequency were not significantly different between schizophrenia and normal subjects. Moreover, no significant difference was found in the promoter polymorphism of GSK-3β in compound genotype distributions and allele frequencies in schizophrenia according to HAM-D scores. However, there was a difference in genotype distribution and allele frequency in schizophrenia according to cognitive impairment. Conclusion: These results suggest that the GSK-3β −50T/C gene polymorphism may be associated with cognitive impairment in patients with schizophrenia.

Abstract

Objective: In this study, authors wanted to find out the association between the glycogen synthase kinase-3β (GSK-3β) −50T/C polymorphism and depression and cognitive impairment in patients with schizophrenia. 207 schizophrenia and 100 normal subjects were participated. We evaluated Brief Psychiatric Rating Scale (BPRS), the Hamilton Depression Rating Scale (HAM-D), and the Korean version of the Mini Mental Status Examination (K-MMSE) in schizophrenia. Methods: Polymerase chain reaction (PCR) analysis of genomic DNA was conducted to evaluate the genotype distribution and allele frequency of GSK-3β −50T/C in subjects. Results: We observed that genotype distribution and allele frequency were not significantly different between schizophrenia and normal subjects. Moreover, no significant difference was found in the promoter polymorphism of GSK-3β in compound genotype distributions and allele frequencies in schizophrenia according to HAM-D scores. However, there was a difference in genotype distribution and allele frequency in schizophrenia according to cognitive impairment. Conclusion: These results suggest that the GSK-3β −50T/C gene polymorphism may be associated with cognitive impairment in patients with schizophrenia.

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