No association between dopamine D3 receptor gene Ser9Gly polymorphism and tardive dyskinesia in schizophrenia
DC Field | Value | Language |
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dc.contributor.author | Lee H.-J. | - |
dc.contributor.author | Kang S.-G. | - |
dc.contributor.author | Choi J.-E. | - |
dc.contributor.author | Park Y.-M. | - |
dc.contributor.author | Lim S.-W. | - |
dc.contributor.author | Kim L. | - |
dc.date.available | 2020-11-03T10:51:54Z | - |
dc.date.issued | 2008-08 | - |
dc.identifier.issn | 1738-1088 | - |
dc.identifier.issn | 2093-4327 | - |
dc.identifier.uri | https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/17405 | - |
dc.description.abstract | Objective: Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotic drug use. Ser9Gly polymorphism of the dopamine 3 receptor (DRD3) has been shown to affect dopamine binding affinity, and may contribute to the susceptibility of antipsychotic-induced TD. This study investigated the possible association between DRD3 gene variant and TD. Methods: We evaluated whether a DRD3 Ser9Gly polymorphism is associated with antipsychotic-induced TD in 209 Korean schizophrenia patients with (n=83) and without TD (n=126) who were matched for antipsychotic drug exposure and other relevant variables. Results: There was no significant association between genotype and allele frequencies determined by the Ser9Gly polymorphism of DRD3 between TD and non-TD patients. In addition, there was no significant difference in terms of total Abnormal Involuntary Movement Scale scores among the three genotype groups. Conclusion: Within the limitations imposed by the size of the clinical sample, these findings suggest that the Ser9Gly polymorphism of DRD3 does not contribute significantly to the risk of TD. Copyright © 2008 Korean College of Neuropsychopharmacology. | - |
dc.format.extent | 4 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.title | No association between dopamine D3 receptor gene Ser9Gly polymorphism and tardive dyskinesia in schizophrenia | - |
dc.type | Article | - |
dc.publisher.location | 대한민국 | - |
dc.identifier.scopusid | 2-s2.0-52149093684 | - |
dc.identifier.bibliographicCitation | Clinical Psychopharmacology and Neuroscience, v.6, no.2, pp 71 - 74 | - |
dc.citation.title | Clinical Psychopharmacology and Neuroscience | - |
dc.citation.volume | 6 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 71 | - |
dc.citation.endPage | 74 | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART001274741 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kciCandi | - |
dc.subject.keywordPlus | atypical antipsychotic agent | - |
dc.subject.keywordPlus | chlorpromazine | - |
dc.subject.keywordPlus | dopamine 3 receptor | - |
dc.subject.keywordPlus | glycine | - |
dc.subject.keywordPlus | neuroleptic agent | - |
dc.subject.keywordPlus | serine | - |
dc.subject.keywordPlus | adult | - |
dc.subject.keywordPlus | article | - |
dc.subject.keywordPlus | controlled study | - |
dc.subject.keywordPlus | drug exposure | - |
dc.subject.keywordPlus | female | - |
dc.subject.keywordPlus | gene frequency | - |
dc.subject.keywordPlus | genetic association | - |
dc.subject.keywordPlus | genetic polymorphism | - |
dc.subject.keywordPlus | genetic risk | - |
dc.subject.keywordPlus | genetic susceptibility | - |
dc.subject.keywordPlus | genetic variability | - |
dc.subject.keywordPlus | genotype | - |
dc.subject.keywordPlus | human | - |
dc.subject.keywordPlus | major clinical study | - |
dc.subject.keywordPlus | male | - |
dc.subject.keywordPlus | mutational analysis | - |
dc.subject.keywordPlus | sample size | - |
dc.subject.keywordPlus | schizophrenia | - |
dc.subject.keywordPlus | South Korea | - |
dc.subject.keywordPlus | tardive dyskinesia | - |
dc.subject.keywordPlus | treatment duration | - |
dc.subject.keywordAuthor | Dopamine 3 receptor | - |
dc.subject.keywordAuthor | Polymorphism | - |
dc.subject.keywordAuthor | Tardive dyskinesia | - |
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