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dc.date.accessioned2017-01-13T12:32:15Z
dc.date.available2017-01-13T12:32:15Z
dc.date.created2016-04-20T14:21:53Z
dc.date.issued2016
dc.identifier.citationHegvik, Tor-Arne Jacobsen, Kaya Kvarme Fredriksen, Mats Zayats, Tetyana Haavik, Jan . A candidate gene investigation of methylphenidate response in adult attention-deficit/hyperactivity disorder patients: results from a naturalistic study. Journal of neural transmission. 2016, 1-7
dc.identifier.urihttp://hdl.handle.net/10852/53524
dc.description.abstractAttention-deficit/hyperactivity disorder (ADHD) is a common childhood onset neuropsychiatric disorder with a complex and heterogeneous symptomatology. Persistence of ADHD symptoms into adulthood is common. Methylphenidate (MPH) is a widely prescribed stimulant compound that may be effective against ADHD symptoms in children and adults. However, MPH does not exert satisfactory effect in all patients. Several genetic variants have been proposed to predict either treatment response or adverse effects of stimulants. We conducted a literature search to identify previously reported variants associated with MPH response and additional variants that were biologically plausible candidates for MPH response. The response to MPH was assessed by the treating clinicians in 564 adult ADHD patients and 20 genetic variants were successfully genotyped. Logistic regression was used to test for association between these polymorphisms and treatment response. Nominal associations (p < 0.05) were meta-analysed with published data from previous comparable studies. In our analyses, rs1800544 in the ADRA2A gene was associated with MPH response at a nominal significance level (OR 0.560, 95 % CI 0.329–0.953, p = 0.033). However, this finding was not affirmed in the meta-analysis. No genetic variants revealed significant associations after correction for multiple testing (p < 0.00125). Our results suggest that none of the studied variants are strong predictors of MPH response in adult ADHD as judged by clinician ratings, potentially except for rs1800544. Consequently, pharmacogenetic testing in routine clinical care is not supported by our analyses. Further studies on the pharmacogenetics of adult ADHD are warranted.en_US
dc.languageEN
dc.language.isoenen_US
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleA candidate gene investigation of methylphenidate response in adult attention-deficit/hyperactivity disorder patients: results from a naturalistic studyen_US
dc.typeJournal articleen_US
dc.creator.authorHegvik, Tor-Arne
dc.creator.authorJacobsen, Kaya Kvarme
dc.creator.authorFredriksen, Mats
dc.creator.authorZayats, Tetyana
dc.creator.authorHaavik, Jan
cristin.unitcode185,90,0,0
cristin.unitnameUniversitetet i Oslo
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1351545
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Journal of neural transmission&rft.volume=&rft.spage=1&rft.date=2016
dc.identifier.jtitleJournal of neural transmission
dc.identifier.volume123
dc.identifier.issue8
dc.identifier.startpage859
dc.identifier.endpage865
dc.identifier.doihttp://dx.doi.org/10.1007/s00702-016-1540-7
dc.identifier.urnURN:NBN:no-56723
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn0300-9564
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/53524/1/253A10.1007-252Fs00702-016-1540-7.pdf
dc.type.versionPublishedVersion


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