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Relationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder

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dc.contributor.authorSoo, Chang H.-
dc.contributor.authorChoi, I.-K.-
dc.contributor.authorLee, H.-Y.-
dc.contributor.authorJeong, Y.-J.-
dc.contributor.authorKim, B.-
dc.contributor.authorLee, M.-S.-
dc.date.accessioned2021-09-06T09:49:27Z-
dc.date.available2021-09-06T09:49:27Z-
dc.date.created2021-06-17-
dc.date.issued2013-
dc.identifier.issn1724-4935-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/105913-
dc.description.abstractObjective: Serotonin 1A receptor (HTR1A) is a candidate molecule for influencing the pathophysiology of major depressive disorder (MDD) and clinical responses to antidepressant treatment. Among polymorphisms of the HTR1A gene, -1019C>G (rs6295) is reportedly a biologically functional polymorphism associated with response to antidepressant treatment. The aim of this study was to determine the relationship between the HTR1A-1019C>G polymorphism and the response to escitalopram in patients with MD. Method: Eighty Korean patients were examined using the Structured Clinical Interview for DSM-IV Axis I disorders and took escitalopram at a daily dose of 5 to 40 mg. Clinical symptoms were evaluated using the 21-item Hamilton Depression Rating (HAM-D) scale during 8 weeks of treatment. The genotypes were determined using HpyCH4 IV digestion following polymerase chain reaction. Results: The proportion of G-allele carriers was 25.0% in responders, which was lower than that in non-responders (53.9%) at 1 week of escitalopram treatment (OR = 0.28, P = 0.030). In allelic analysis, the frequency of the G allele was significantly lower in responders at 1 week than in non-responders (12.5% versus 31.7%, respectively; OR = 0.29, P = 0.029). Similarly, the ratio of HAM-D score at 1 week to the baseline score in C-allele carriers was 67.6% ± 2.42%, which was significantly lower than the ratio of 75.8% ± 2.74% in patients possessing the G allele (P = 0.027). Conclusions: Although this study is preliminary and has several limitations, our results suggest that HTR1A- 1019C>G may be a genetic marker predicting the response to escitalopram treatment. © 2013 Giovanni Fioriti Editore s.r.l.-
dc.languageEnglish-
dc.language.isoen-
dc.subjectcytosine-
dc.subjectescitalopram-
dc.subjectguanine-
dc.subjectrestriction endonuclease-
dc.subjectserotonin 1A receptor-
dc.subjectadult-
dc.subjectaged-
dc.subjectallele-
dc.subjectarticle-
dc.subjectdisease severity-
dc.subjectDNA extraction-
dc.subjectfemale-
dc.subjectgene amplification-
dc.subjectgene expression-
dc.subjectgenetic analysis-
dc.subjectgenetic association-
dc.subjectgenetic marker-
dc.subjectgenetic polymorphism-
dc.subjectgenetic variability-
dc.subjectgenotype-
dc.subjectHamilton scale-
dc.subjectheterozygote-
dc.subjectHTR1A gene-
dc.subjecthuman-
dc.subjectmajor clinical study-
dc.subjectmajor depression-
dc.subjectmale-
dc.subjectpharmacogenetics-
dc.subjectpolymerase chain reaction-
dc.subjectremission-
dc.subjectsingle nucleotide polymorphism-
dc.subjectStructured Clinical Interview for DSM Disorders-
dc.subjectsymptom assessment-
dc.subjecttreatment response-
dc.titleRelationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, M.-S.-
dc.identifier.scopusid2-s2.0-84885042242-
dc.identifier.bibliographicCitationClinical Neuropsychiatry, v.10, no.3-4, pp.148 - 154-
dc.relation.isPartOfClinical Neuropsychiatry-
dc.citation.titleClinical Neuropsychiatry-
dc.citation.volume10-
dc.citation.number3-4-
dc.citation.startPage148-
dc.citation.endPage154-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPluscytosine-
dc.subject.keywordPlusescitalopram-
dc.subject.keywordPlusguanine-
dc.subject.keywordPlusrestriction endonuclease-
dc.subject.keywordPlusserotonin 1A receptor-
dc.subject.keywordPlusadult-
dc.subject.keywordPlusaged-
dc.subject.keywordPlusallele-
dc.subject.keywordPlusarticle-
dc.subject.keywordPlusdisease severity-
dc.subject.keywordPlusDNA extraction-
dc.subject.keywordPlusfemale-
dc.subject.keywordPlusgene amplification-
dc.subject.keywordPlusgene expression-
dc.subject.keywordPlusgenetic analysis-
dc.subject.keywordPlusgenetic association-
dc.subject.keywordPlusgenetic marker-
dc.subject.keywordPlusgenetic polymorphism-
dc.subject.keywordPlusgenetic variability-
dc.subject.keywordPlusgenotype-
dc.subject.keywordPlusHamilton scale-
dc.subject.keywordPlusheterozygote-
dc.subject.keywordPlusHTR1A gene-
dc.subject.keywordPlushuman-
dc.subject.keywordPlusmajor clinical study-
dc.subject.keywordPlusmajor depression-
dc.subject.keywordPlusmale-
dc.subject.keywordPluspharmacogenetics-
dc.subject.keywordPluspolymerase chain reaction-
dc.subject.keywordPlusremission-
dc.subject.keywordPlussingle nucleotide polymorphism-
dc.subject.keywordPlusStructured Clinical Interview for DSM Disorders-
dc.subject.keywordPlussymptom assessment-
dc.subject.keywordPlustreatment response-
dc.subject.keywordAuthorEscitalopram-
dc.subject.keywordAuthorMajor depressive disorder-
dc.subject.keywordAuthorSerotonin receptor 1A-
dc.subject.keywordAuthorSingle-nucleotide polymorphism-
dc.subject.keywordAuthorTreatment response-
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