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Heilbronner, Urs
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Heilbronner, Urs
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Heilbronner, Urs
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Heilbronner, U.
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2016Journal Article [["dc.bibliographiccitation.firstpage","1085"],["dc.bibliographiccitation.issue","10023"],["dc.bibliographiccitation.journal","The Lancet"],["dc.bibliographiccitation.lastpage","1093"],["dc.bibliographiccitation.volume","387"],["dc.contributor.author","Hou, Liping"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Adli, Mazda"],["dc.contributor.author","Akiyama, Kazufumi"],["dc.contributor.author","Akula, Nirmala"],["dc.contributor.author","Ardau, Raffaella"],["dc.contributor.author","Arias, Bárbara"],["dc.contributor.author","Backlund, Lena"],["dc.contributor.author","Banzato, Claudio E M"],["dc.contributor.author","Schulze, Thomas G"],["dc.date.accessioned","2020-12-10T15:21:52Z"],["dc.date.available","2020-12-10T15:21:52Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/S0140-6736(16)00143-4"],["dc.identifier.issn","0140-6736"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73198"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Genetic variants associated with response to lithium treatment in bipolar disorder: a genome-wide association study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2019Journal Article [["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.lastpage","75"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Kalman, Janos L."],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Adli, Mazda"],["dc.contributor.author","Adorjan, Kristina"],["dc.contributor.author","Akula, Nirmala"],["dc.contributor.author","Alda, Martin"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2019-07-09T11:50:29Z"],["dc.date.available","2019-07-09T11:50:29Z"],["dc.date.issued","2019"],["dc.description.abstract","OBJECTIVES: Bipolar disorder (BD) with early disease onset is associated with an unfavorable clinical outcome and constitutes a clinically and biologically homogenous subgroup within the heterogeneous BD spectrum. Previous studies have found an accumulation of early age at onset (AAO) in BD families and have therefore hypothesized that there is a larger genetic contribution to the early-onset cases than to late onset BD. To investigate the genetic background of this subphenotype, we evaluated whether an increased polygenic burden of BD- and schizophrenia (SCZ)-associated risk variants is associated with an earlier AAO in BD patients. METHODS: A total of 1995 BD type 1 patients from the Consortium of Lithium Genetics (ConLiGen), PsyCourse and Bonn-Mannheim samples were genotyped and their BD and SCZ polygenic risk scores (PRSs) were calculated using the summary statistics of the Psychiatric Genomics Consortium as a training data set. AAO was either separated into onset groups of clinical interest (childhood and adolescence [≤18 years] vs adulthood [>18 years]) or considered as a continuous measure. The associations between BD- and SCZ-PRSs and AAO were evaluated with regression models. RESULTS: BD- and SCZ-PRSs were not significantly associated with age at disease onset. Results remained the same when analyses were stratified by site of recruitment. CONCLUSIONS: The current study is the largest conducted so far to investigate the association between the cumulative BD and SCZ polygenic risk and AAO in BD patients. The reported negative results suggest that such a polygenic influence, if there is any, is not large, and highlight the importance of conducting further, larger scale studies to obtain more information on the genetic architecture of this clinically relevant phenotype."],["dc.identifier.doi","10.1111/bdi.12659"],["dc.identifier.pmid","29956436"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15948"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59781"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1399-5618"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Investigating polygenic burden in age at disease onset in bipolar disorder: Findings from an international multicentric study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2021Journal Article [["dc.bibliographiccitation.firstpage","80"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Complex Psychiatry"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Coombes, Brandon J."],["dc.contributor.author","Millischer, Vincent"],["dc.contributor.author","Batzler, Anthony"],["dc.contributor.author","Larrabee, Beth"],["dc.contributor.author","Hou, Liping"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Adli, Mazda"],["dc.contributor.author","Akiyama, Kazufumi"],["dc.contributor.author","Akula, Nirmala"],["dc.contributor.author","Biernacka, Joanna M."],["dc.date.accessioned","2022-12-01T08:31:18Z"],["dc.date.available","2022-12-01T08:31:18Z"],["dc.date.issued","2021"],["dc.description.abstract","Response to lithium varies widely between individuals with bipolar disorder (BD). Polygenic risk scores (PRSs) can uncover pharmacogenomics effects and may help predict drug response. Patients (N = 2,510) with BD were assessed for long-term lithium response in the Consortium on Lithium Genetics using the Retrospective Criteria of Long-Term Treatment Response in Research Subjects with Bipolar Disorder score. PRSs for attention-deficit/hyperactivity disorder (ADHD), major depressive disorder (MDD), and schizophrenia (SCZ) were computed using lassosum and in a model including all three PRSs and other covariates, and the PRS of ADHD (β = −0.14; 95% confidence interval [CI]: −0.24 to −0.03; p value = 0.010) and MDD (β = −0.16; 95% CI: −0.27 to −0.04; p value = 0.005) predicted worse quantitative lithium response. A higher SCZ PRS was associated with higher rates of medication nonadherence (OR = 1.61; 95% CI: 1.34–1.93; p value = 2e−7). This study indicates that genetic risk for ADHD and depression may influence lithium treatment response. Interestingly, a higher SCZ PRS was associated with poor adherence, which can negatively impact treatment response. Incorporating genetic risk of ADHD, depression, and SCZ in combination with clinical risk may lead to better clinical care for patients with BD."],["dc.identifier.doi","10.1159/000519707"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118136"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","2673-298X"],["dc.relation.issn","2673-3005"],["dc.title","Association of Attention-Deficit/Hyperactivity Disorder and Depression Polygenic Scores with Lithium Response: A Consortium for Lithium Genetics Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI