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dc.contributor.authorAarsland, Tore Ivar Malmeien_US
dc.contributor.authorLeskauskaite, Ievaen_US
dc.contributor.authorMidttun, Øivinden_US
dc.contributor.authorUlvik, Arveen_US
dc.contributor.authorUeland, Per Magneen_US
dc.contributor.authorOltedal, Leifen_US
dc.contributor.authorErchinger, Vera Janeen_US
dc.contributor.authorØdegaard, Ketil Joachimen_US
dc.contributor.authorHaavik, Janen_US
dc.contributor.authorKessler, Uteen_US
dc.date.accessioned2020-05-25T13:16:08Z
dc.date.available2020-05-25T13:16:08Z
dc.date.issued2019-05-31
dc.identifier.issn1935-861X
dc.identifier.issn1876-4754
dc.identifier.urihttps://hdl.handle.net/1956/22367
dc.description.abstractBackground: Prior studies suggest that activation of the tryptophan catabolism via the kynurenine pathway by proinflammatory cytokines may be involved in the pathophysiology of depression. Electroconvulsive therapy (ECT) is an effective treatment for major depression (MD) with immunomodulation as one of the proposed modes of action. Objective: The aim of this study was to investigate serum concentrations of tryptophan and kynurenine pathway metabolites in MD patients and healthy controls, and to explore the effect of ECT on components of the kynurenine pathway. Methods: The study included 27 moderately to severely depressed patients referred to ECT. Blood samples were collected prior to treatment and after the completed ECT-series. Baseline samples were also collected from 14 healthy, age- and sex-matched controls. Serum concentrations of tryptophan, kynurenine, 3-hydroxykynurenine (HK), kynurenic acid (KA), xanthurenic acid (XA), anthranilic acid (AA), 3-hydroxyanthranilic acid (HAA), quinolinic acid (QA), picolinic acid (Pic), pyridoxal 5′-phosphat (PLP), riboflavin, neopterin and cotinine were measured. Results: Patients with MD had lower levels of neuroprotective kynurenine-pathway metabolites (KA, XA and Pic) and lower metabolite ratios (KA/Kyn and KA/QA) reflecting reduced neuroprotection compared to controls. The concentration of the inflammatory marker neopterin was increased after ECT, along with Pic and the redox active and immunosuppressive metabolite HAA. Conclusion: In this pilot study, we found increased concentrations of inflammatory marker neopterin and putative neuroprotective kynurenine metabolites HAA and Pic in MD patients after ECT. Further research in larger cohorts is required to conclude whether ECT exerts its therapeutic effects via changes in the kynurenine pathway.en_US
dc.language.isoengeng
dc.publisherElseviereng
dc.rightsAttribution-NonCommercial-NoDerivs CC BY-NC-NDeng
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/eng
dc.subjectECTeng
dc.subjectDepressioneng
dc.subjectTryptophaneng
dc.subjectKynurenineeng
dc.subjectInflammationeng
dc.titleThe effect of electroconvulsive therapy (ECT) on serum tryptophan metabolitesen_US
dc.typePeer reviewed
dc.typeJournal article
dc.date.updated2019-11-15T11:37:45Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2019 The Author(s)
dc.identifier.doihttps://doi.org/10.1016/j.brs.2019.05.018
dc.identifier.cristin1709504
dc.source.journalBrain Stimulation
dc.source.pagenumber1135-1142
dc.identifier.citationBrain Stimulation. 2019, 12 (5), 1135-1142.
dc.source.volume12
dc.source.issue5


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