Eichhammer, Peter and Albus, M. and Borrmann-Hassenbach, M. and Schoeler, A. and Putzhammer, A. and Frick, U. and Klein, H. E. and Rohrmeier, T. (2000) Association of dopamine D3-receptor gene variants with neuroleptic induced akathisia in schizophrenic patients: A generalization of Steen's study on DRD3 and tardive dyskinesia. AMERICAN JOURNAL OF MEDICAL GENETICS, 96 (2). pp. 187-191. ISSN 0148-7299
Full text not available from this repository. (Request a copy)Abstract
Neuroleptic induced akathisia is a common and distressful extrapyramidal side effect of antipsychotic treatment, A significant proportion of the variability of its development has been left unexplained and has to be attributed to individual susceptibility. Since hereditary factors have been discussed in the etiology of acute akathisia (AA), part of the individual susceptibility might be of genetic origin, Moreover, AA is regarded as a forerunner of tardive dyskinesia, a drug-induced chronic movement disorder, which may be associated with homozygosity for the Ser9Gly variant of the DRD3 gene. Considering expression studies, which demonstrated functional variants of DRD3 polymorphisms, we investigated whether homozygosity for the Ser9Gly variant of the DRD3 gene is associated with AA, Homozygosity for the Ser9Gly variant of the DRD3 gene was connected to an 88% incidence of AA as compared with a considerably lower 46.9% incidence of AA in schizophrenic patients nonhomozygous for the 2-2 allele (exact P = 0.0223). (C) 2000 Wiley-Liss, Inc.
Item Type: | Article |
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Uncontrolled Keywords: | DRUG-INDUCED AKATHISIA; D3 RECEPTOR GENE; CLINICAL CHARACTERISTICS; EXTRAPYRAMIDAL SIGNS; LOCOMOTOR-ACTIVITY; PREVALENCE; CLOZAPINE; SYMPTOMS; SYSTEM; IRON; akathisia; risk factors; dopamine D3 receptor variant |
Subjects: | 600 Technology > 610 Medical sciences Medicine |
Divisions: | Medicine > Lehrstuhl für Psychiatrie und Psychotherapie |
Depositing User: | Dr. Gernot Deinzer |
Date Deposited: | 16 May 2022 09:33 |
Last Modified: | 16 May 2022 09:33 |
URI: | https://pred.uni-regensburg.de/id/eprint/42589 |
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