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Title: Susceptibility to neuroleptic-induced tardive dyskinesia and the T102C polymorphism in the serotonin type 2A receptor
Authors: Tan, E.-C.
Chong, S.-A.
Mahendran, R.
Dong, F. 
Tan, C.-H.
Keywords: Polymorphism
Serotonin receptor gene
Tardive dyskinesia
Issue Date: 15-Jul-2001
Source: Tan, E.-C., Chong, S.-A., Mahendran, R., Dong, F., Tan, C.-H. (2001-07-15). Susceptibility to neuroleptic-induced tardive dyskinesia and the T102C polymorphism in the serotonin type 2A receptor. Biological Psychiatry 50 (2) : 144-147. ScholarBank@NUS Repository.
Abstract: Background: Genetic factors have been implicated in the pathophysiology of the movement disorder tardive dyskinesia, which may involve dopamine-serotonin interaction. Case-control association studies have identified the T102C polymorphism of the 5-HT2A receptor gene as being associated with schizophrenia and responsiveness to clozapine. In this study, we examine the association of this polymorphism in the 5-HT2A receptor gene as a risk factor for developing schizophrenia and tardive dyskinesia from prolonged treatment with neuroleptics. Methods: Ninety-seven healthy control subjects with no history of mental illness and 221 schizophrenic patients (87 with tardive dyskinesia, 134 without) were genotyped by PCR-RFLP. Results: Comparison between cases and control subjects revealed no significant association between the C allele and schizophrenia. There was significant difference in allele frequency (p = .044, OR = 1.54 95% CI = 1.02-2.33) between patients who developed tardive dyskinesia and those who did not. Significant difference remains even after adjusting for age and neuroleptic dosage (p = .041) with the odds ratio at 1.64 (95% CI = 1.02-2.62). Conclusions: A genetic variant of the 5-HT2A receptor may be associated with neuroleptic-induced tardive dyskinesia in schizophrenia. Further studies are needed to replicate the finding. The role of 5-HT2A receptor in the etiology of tardive dyskinesia or treatment-resistant schizophrenia should be further investigated. © 2001 Society of Biological Psychiatry.
Source Title: Biological Psychiatry
ISSN: 00063223
DOI: 10.1016/S0006-3223(01)01076-9
Appears in Collections:Staff Publications

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