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An investigation of the α 1A ‐adrenergic receptor gene and antipsychotic‐induced side‐effects
Author(s) -
Saiz Pilar A.,
Susce Margaret T.,
Clark Dan A.,
Kerwin Robert W.,
Molero Patricio,
Arranz Maria J.,
de Leon Jose
Publication year - 2008
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.903
Subject(s) - antipsychotic , tardive dyskinesia , side effect (computer science) , medicine , pharmacology , extrapyramidal symptoms , pharmacogenomics , atypical antipsychotic , sedation , schizophrenia (object oriented programming) , psychiatry , computer science , programming language
Antipsychotic treatment is hampered by the induction of side‐effects such as tardive dyskinesia (TD), weight gain, sedation and extrapyramidal side‐effects (EPS). Identification of the factors related to their development would facilitate their avoidance and the improvement of antipsychotic treatment. It has been hypothesised that genetic variants in drug targeted receptors may contribute to the development of side‐effects. In this study, we have investigated the possible influence of genetic variants (‐563‐C/T, ‐4155‐G/C and ‐4884‐A/G) of the α 1A ‐adrenergic receptor, an important target of atypical antipsychotic drugs, and development of side‐effects after antipsychotic medication in a sample of N = 427 US Caucasian patients. We found several marginal associations ( p < 0.05) between α 1A ‐adrenergic genetic variants and antipsychotic‐induced side‐effects which did not reach statistical significance after corrections for multiple analyses. These results do not support a major role of α 1A ‐adrenergic genetic variants in obesity and other side‐effects observed after prolonged treatment with antipsychotic medications. Copyright © 2007 John Wiley & Sons, Ltd.