Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/96426
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dc.contributor.authorDomschke, K.en
dc.contributor.authorTidow, N.en
dc.contributor.authorSchwarte, K.en
dc.contributor.authorZiegler, C.en
dc.contributor.authorLesch, K.en
dc.contributor.authorDeckert, J.en
dc.contributor.authorArolt, V.en
dc.contributor.authorZwanzger, P.en
dc.contributor.authorBaune, B.en
dc.date.issued2015en
dc.identifier.citationJournal of Neural Transmission, 2015; 122(1):99-108en
dc.identifier.issn0300-9564en
dc.identifier.issn1435-1463en
dc.identifier.urihttp://hdl.handle.net/2440/96426-
dc.descriptionFirst online: 10 May 2014en
dc.description.abstractThe monoamine oxidase A (MAO-A) gene has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of major depressive disorder. In the present analysis, for the first time a pharmacoepigenetic approach was applied investigating the influence of DNA methylation patterns in the MAO-A regulatory and exon1/intron1 region on antidepressant treatment response. 94 patients of Caucasian descent with major depressive disorder (f = 61; DSM-IV) were analyzed for DNA methylation status at 43 MAO-A CpG sites via direct sequencing of sodium bisulfite treated DNA extracted from blood cells. Patients were also genotyped for the functional MAO-A VNTR. Clinical response to antidepressant treatment with escitalopram was assessed by intra-individual changes of HAM-D-21 scores after 6 weeks of treatment. Apart from two CpG sites, male subjects showed no or only very minor methylation. In female patients, lower methylation at two individual CpG sites in the MAO-A promoter region was nominally associated with impaired response to antidepressant treatment after 6 weeks (GRCh37/hg19: CpG 43.514.063, p = 0.04; CpG 43.514.684, p = 0.009), not, however, withstanding correction for multiple testing. MAO-A VNTR genotypes did not influence MAO-A methylation status. The present pilot data do not suggest a major influence of MAO-A DNA methylation on antidepressant treatment response. However, the presently observed trend towards CpG-specific MAO-A gene hypomethylation-possibly via increased gene expression and consecutively decreased serotonin and/or norepinephrine availability-to potentially drive impaired antidepressant treatment response in female patients might be worthwhile to be followed up in larger pharmacoepigenetic studies.en
dc.description.statementofresponsibilityKatharina Domschke, Nicola Tidow, Kathrin Schwarte, Christiane Ziegler, Klaus-Peter Lesch, Jürgen Deckert, Volker Arolt, Peter Zwanzger, Bernhard T. Bauneen
dc.language.isoenen
dc.publisherSpringer-Verlagen
dc.rights© Springer-Verlag Wien 2014en
dc.subjectMonoamine oxidase A; Epigenetics; Pharmacoepigenetics; Methylation; Depression; Genderen
dc.titlePharmacoepigenetics of depression: no major influence of MAO-A DNA methylation on treatment responseen
dc.typeJournal articleen
dc.identifier.rmid0030023094en
dc.identifier.doi10.1007/s00702-014-1227-xen
dc.identifier.pubid139150-
pubs.library.collectionPsychiatry publicationsen
pubs.library.teamDS03en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidBaune, B. [0000-0001-6548-426X]en
Appears in Collections:Psychiatry publications

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