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Tardive dyskinesia is not associated with the polymorphisms of 5-HT2A receptor gene, serotonin transporter gene and catechol-o-methyltransferase gene ⋆

Published online by Cambridge University Press:  16 April 2020

Hasan Herken ,
M. Emin Erdal ,
Ömer Böke  and
Haluk A. Savaş
Hasan Herken*
Affiliation:
Department of Psychiatry, Medical Faculty of Gaziantep University, Gaziantep City, Turkey
M. Emin Erdal
Affiliation:
Samsun Mental Hospital, Turkey
Ömer Böke
Affiliation:
Department of Medical Biology and Genetics, Medical Facultyof Mersin University, Turkey
Haluk A. Savaş
Affiliation:
Department of Psychiatry, Medical Faculty of Gaziantep University, Gaziantep City, Turkey
*
*E-mail address: hasanherken@hotmail.com
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Abstract

Background

The pathophysiology of tardive dyskinesia (TD) is not completely understood.

Aim

To assess the relationship of TD with 5-HT2A receptor gene, serotonin transporter gene (5 HTT), and catechol-o-methyltransferase (COMT) gene polymorphisms.

Methods

Our study comprised 111 unrelated subjects who strictly met DSM-IV criteria for schizophrenia and 32 TD, and 79 healthy unrelated controls; all the subjects were of Turkish origin. The analyses of 5-HT2A receptor gene, 5 HTT gene, and COMT gene polymorphisms were performed using polymerase chain reaction (PCR) technique.

Results

The polymorphisms of these genes were not significantly different between the schizophrenic patients, TD and control subjects.

Conclusions

Our findings indicated that 5-HT2A receptor gene, 5 HTT gene, and COMT gene polymorphisms were similar in schizophrenia with non-TD, schizophrenia with TD, and healthy controls. These polymorphisms, though, do not help to evaluate the susceptibility to TD.

Keywords

Tardive dyskinesia5-HT2A receptor geneCOMT gene5 HTT geneSchizophrenia
Type
Original article
Information
European Psychiatry , Volume 18 , Issue 2 , March 2003 , pp. 77 - 81
Copyright
Copyright © Éditions scientifiques et médicales Elsevier SAS 2002

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Footnotes

This study was partly presented at the III National Congress of Biological Psychiatry, 18–20 June 2000, Cappadocia, Turkey.

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