Heilbronner, Urs

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Reinbold, Céline S."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Hecker, Julian"],["dc.contributor.author","Fullerton, Janice M."],["dc.contributor.author","Hoffmann, Per"],["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","Cichon, Sven"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2020-12-10T18:46:52Z"],["dc.date.available","2020-12-10T18:46:52Z"],["dc.date.issued","2018"],["dc.description.abstract","Bipolar disorder (BD) is a common, highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. Lithium is the best-established long-term treatment for BD, even though individual response is highly variable. Evidence suggests that some of this variability has a genetic basis. This is supported by the largest genome-wide association study (GWAS) of lithium response to date conducted by the International Consortium on Lithium Genetics (ConLiGen). Recently, we performed the first genome-wide analysis of the involvement of miRNAs in BD and identified nine BD-associated miRNAs. However, it is unknown whether these miRNAs are also associated with lithium response in BD. In the present study, we therefore tested whether common variants at these nine candidate miRNAs contribute to the variance in lithium response in BD. Furthermore, we systematically analyzed whether any other miRNA in the genome is implicated in the response to lithium. For this purpose, we performed gene-based tests for all known miRNA coding genes in the ConLiGen GWAS dataset (n = 2,563 patients) using a set-based testing approach adapted from the versatile gene-based test for GWAS (VEGAS2). In the candidate approach, miR-499a showed a nominally significant association with lithium response, providing some evidence for involvement in both development and treatment of BD. In the genome-wide miRNA analysis, 71 miRNAs showed nominally significant associations with the dichotomous phenotype and 106 with the continuous trait for treatment response. A total of 15 miRNAs revealed nominal significance in both phenotypes with miR-633 showing the strongest association with the continuous trait (p = 9.80E-04) and miR-607 with the dichotomous phenotype (p = 5.79E-04). No association between miRNAs and treatment response to lithium in BD in either of the tested conditions withstood multiple testing correction. Given the limited power of our study, the investigation of miRNAs in larger GWAS samples of BD and lithium response is warranted."],["dc.identifier.doi","10.3389/fpsyt.2018.00207"],["dc.identifier.eissn","1664-0640"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78571"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Analysis of the Influence of microRNAs in Lithium Response in Bipolar Disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","2262"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","2270"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Malzahn, Dorthe"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Maier, Sandra"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2018-11-07T09:48:13Z"],["dc.date.available","2018-11-07T09:48:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Sex is a powerful modulator of disease susceptibility, course and outcome. The gene CACNA1C is among the best replicated vulnerability genes of bipolar disorder and schizophrenia. The aim of the present study was to investigate whether sex and a variant in CACNA1C (rs10774035 as a proxy for the well-acknowledged risk variant rs1006737) influence psychosocial adaptation in a Large German patient sample with schizophrenia-spectrum (n=297) and bipolar (n=516) disorders. We analyzed Global Assessment of Functioning (GAF) scores, retrospectively collected for different time points during disease course. We investigated whether CACNA1C sex-dependently modulates longitudinal GAF scores and recovery from episodes of psychiatric disturbance in the above mentioned disorders. Psychosocial recovery was measured as difference score between the current GAF score (assessing the last remission) and the worst GAF score ever during an illness episode. Covariate- adjusted association analyses revealed a sex x rs10774035 genotype interaction on longitudinal GAF and recovery from illness episodes only in schizophrenia-spectrum but not in bipolar disorders. In schizophrenia-spectrum affected mates, rs10774035 minor allele (T) carriers had higher GAF scores at three time points (premorbid, worst ever, current). In contrast, females carrying rs10774035 minor alleles had impaired recovery from schizophrenia-spectrum episodes. These results encourage further investigations of gene x sex interactions and longitudinal quantitative phenotypes to unravel the rich variety of behavioral consequences of genetic individuality. (C) 2015 Elsevier B.V. and ECNP. All rights reserved."],["dc.identifier.doi","10.1016/j.euroneuro.2015.09.012"],["dc.identifier.isi","000366947300008"],["dc.identifier.pmid","26475575"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12743"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35259"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-7862"],["dc.relation.issn","0924-977X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A common risk variant in CACNA1C supports a sex-dependent effect on longitudinal functioning and functional recovery from episodes of schizophrenia-spectrum but not bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Comes, Ashley L."],["dc.contributor.author","Senner, Fanny"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Adorjan, Kristina"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Andlauer, Till F. M."],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Hake, Maria"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Kalman, Janos L."],["dc.contributor.author","Reich-Erkelenz, Daniela"],["dc.contributor.author","Klöhn-Saghatolislam, Farah"],["dc.contributor.author","Schaupp, Sabrina K."],["dc.contributor.author","Schulte, Eva C."],["dc.contributor.author","Juckel, Georg"],["dc.contributor.author","Dannlowski, Udo"],["dc.contributor.author","Schmauß, Max"],["dc.contributor.author","Zimmermann, Jörg"],["dc.contributor.author","Reimer, Jens"],["dc.contributor.author","Reininghaus, Eva"],["dc.contributor.author","Anghelescu, Ion‐George"],["dc.contributor.author","Arolt, Volker"],["dc.contributor.author","Baune, Bernhard T."],["dc.contributor.author","Konrad, Carsten"],["dc.contributor.author","Thiel, Andreas"],["dc.contributor.author","Fallgatter, Andreas J."],["dc.contributor.author","Nieratschker, Vanessa"],["dc.contributor.author","Figge, Christian"],["dc.contributor.author","von Hagen, Martin"],["dc.contributor.author","Koller, Manfred"],["dc.contributor.author","Becker, Thomas"],["dc.contributor.author","Wigand, Moritz E."],["dc.contributor.author","Jäger, Markus"],["dc.contributor.author","Dietrich, Detlef E."],["dc.contributor.author","Stierl, Sebastian"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Spitzer, Carsten"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Papiol, Sergi"],["dc.date.accessioned","2020-12-10T18:09:40Z"],["dc.date.available","2020-12-10T18:09:40Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41398-019-0547-x"],["dc.identifier.eissn","2158-3188"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16411"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73721"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The genetic relationship between educational attainment and cognitive performance in major psychiatric disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]