No evidence for an association between G protein β3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia

Na, Kyoung-Sae; Paik, Jong Woo; Lee, Moon Soo; Cho, Bang Hyun; Park, Young Min; Kim, Won; Choi, Jung Eun; Jung, In Kwa; Lee, Heon Jeong; Lee, Min Soo

doi:10.1002/hup.875

Cited by 19 publications

(7 citation statements)

References 15 publications

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“…All of the subjects were inpatients at the three collaborating hospitals. Other findings from these subjects have been reported previously (Kang et al, 2008a(Kang et al, , 2008bLee et al, 2007aLee et al, , 2007b.…”

Section: Study Subjectssupporting

confidence: 86%

Association study between glutathione S‐transferase GST‐M1, GST‐T1, and GST‐P1 polymorphisms and tardive dyskinesia

Lee

Choi

et al. 2008

Human Psychopharmacology

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Section: Study Subjectssupporting

confidence: 86%

Association study between glutathione S‐transferase GST‐M1, GST‐T1, and GST‐P1 polymorphisms and tardive dyskinesia

Lee

Choi

et al. 2008

Human Psychopharmacology

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“…All subjects had been maintained on stable dosages of antipsychotics for at least 3 months prior to the assessment of TD. Other findings from these subjects have been reported previously [17][18][19] . We rated the first 7 items of the AIMS to determine the total AIMS score for abnormal movements.…”

Section: Methodssupporting

confidence: 63%

Val158Met Polymorphism in the Catechol-O-Methyltransferase (COMT) Gene Is Not Associated with Tardive Dyskinesia in Schizophrenia

Na¹,

Choi²,

Park

et al. 2008

Neuropsychobiology

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Objective: This study investigated whether the catechol-O-methyltransferase (COMT) gene V158M single-nucleotide polymorphism (SNP) influences susceptibility to tardive dyskinesia (TD). Methods: We examined 209 Korean schizophrenic patients using the Abnormal Involuntary Movement Scale (AIMS), with genotyping performed for the COMT gene V158M SNP. Results: The logistic regression analysis showed that old age [p = 0.032, OR = 1.40 (OR corresponds to 10-year), 95% CI = 1.03–1.90] was a risk factor for TD, but there was no significant association between the COMT genotype and TD. The heterozygotes (MV genotype) of the COMT gene polymorphism tended to develop TD less than homozygotes (MM and VV); however, the risk did not reach statistical significance (p = 0.050, OR = 1.81, 95% CI = 1.00–3.29). Conclusions: These results suggest that the V158M SNP of the COMT gene is not associated with TD in schizophrenia. However, there is a tendency that the heterozygous genotype of the COMT gene polymorphism has a protective effect against TD. Further investigations are warranted to evaluate a molecular heterosis of this polymorphism in development of TD in a large sample of subjects.

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“…A Korean case-control study examining the G-protein beta3 subunit gene found no association between the C825T polymorphism and TD. 155 In contrast, a case-control study found the AGG haplotype is significantly associated with TD phenotype ( P =0.007). 27 To date, the function of this haplotype is unknown and this result is yet to be replicated.…”

Section: Resultsmentioning

confidence: 93%

Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

Chang

Fung

2014

PGPM

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Pharmacogenomics is the study of the effects of genetic polymorphisms on medication pharmacokinetics and pharmacodynamics. It offers advantages in predicting drug efficacy and/or toxicity and has already changed clinical practice in many fields of medicine. Tardive dyskinesia (TD) is a movement disorder that rarely remits and poses significant social stigma and physical discomfort for the patient. Pharmacokinetic studies show an association between cytochrome P450 enzyme-determined poor metabolizer status and elevated serum antipsychotic and metabolite levels. However, few prospective studies have shown this to correlate with the occurrence of TD. Many retrospective, case-control and cross-sectional studies have examined the association of cytochrome P450 enzyme, dopamine (receptor, metabolizer and transporter), serotonin (receptor and transporter), and oxidative stress enzyme gene polymorphisms with the occurrence and severity of TD. These studies have produced conflicting and confusing results secondary to heterogeneous inclusion criteria and other patient characteristics that also act as confounding factors. This paper aims to review and summarize the pharmacogenetic findings in antipsychotic-associated TD and assess its clinical significance for psychiatry patients. In addition, we hope to provide insight into areas that need further research.

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No evidence for an association between G protein β3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia

Abstract: Within the limitations imposed by the size of the clinical sample, these findings suggest that the GNB3 825 C/T single nucleotide polymorphism (SNP) does not contribute significantly to risk for TD.

Cited by 19 publications

References 15 publications

Association study between glutathione S‐transferase GST‐M1, GST‐T1, and GST‐P1 polymorphisms and tardive dyskinesia

Association study between glutathione S‐transferase GST‐M1, GST‐T1, and GST‐P1 polymorphisms and tardive dyskinesia

Val158Met Polymorphism in the Catechol-<i>O</i>-Methyltransferase (<i>COMT)</i> Gene Is Not Associated with Tardive Dyskinesia in Schizophrenia

Clinical significance of pharmacogenomic studies in tardive dyskinesia associated with patients with psychiatric disorders

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