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.artnumber","e55"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","BJPsych Open"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Stahl, Katharina"],["dc.contributor.author","Adorjan, Kristina"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Comes, Ashley L."],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Heilbronner, Maria"],["dc.contributor.author","Kalman, Janos L."],["dc.contributor.author","Klöhn-Saghatolislam, Farahnaz"],["dc.contributor.author","Oraki Kohshour, Mojtaba"],["dc.contributor.author","Heilbronner, Urs"],["dc.date.accessioned","2022-04-01T10:02:14Z"],["dc.date.available","2022-04-01T10:02:14Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Case-only longitudinal studies are common in psychiatry. Further, it is assumed that psychiatric ratings and questionnaire results of healthy controls stay stable over foreseeable time ranges. For cognitive tests, improvements over time are expected, but data for more than two administrations are scarce. Aims We comprehensively investigated the longitudinal course for trends over time in cognitive and symptom measurements for severe mental disorders. Assessments included the Trail Making Tests, verbal Digit Span tests, Global Assessment of Functioning, Inventory of Depressive Symptomatology, the Positive and Negative Syndrome Scale, and the Young Mania Rating Scale, among others. Method Using the data of control individuals ( n = 326) from the PsyCourse study who had up to four assessments over 18 months, we modelled the course using linear mixed models or logistic regression. The slopes or odds ratios were estimated and adjusted for age and gender. We also assessed the robustness of these results using a longitudinal non-parametric test in a sensitivity analysis. Results Small effects were detected for most cognitive tests, indicating a performance improvement over time ( P < 0.05). However, for most of the symptom rating scales and questionnaires, no effects were detected, in line with our initial hypothesis. Conclusions The slightly but consistently improved performance in the cognitive tests speaks of a test-unspecific positive trend, while psychiatric ratings and questionnaire results remain stable over the observed period. These detectable improvements need to be considered when interpreting longitudinal courses. We therefore recommend recruiting control participants if cognitive tests are administered."],["dc.identifier.doi","10.1192/bjo.2022.17"],["dc.identifier.pii","S2056472422000175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105856"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2056-4724"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Stability over time of scores on psychiatric rating scales, questionnaires and cognitive tests in healthy controls"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","386"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Wendel, Bernadette"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Andlauer, Till F. M."],["dc.contributor.author","Zimmermann, Jörg"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Spitzer, Carsten"],["dc.contributor.author","Senner, Fanny"],["dc.contributor.author","Schulte, Eva C."],["dc.contributor.author","Schmauß, Max"],["dc.contributor.author","Heilbronner, Urs"],["dc.date.accessioned","2021-08-12T07:44:54Z"],["dc.date.available","2021-08-12T07:44:54Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Executive functions are metacognitive capabilities that control and coordinate mental processes. In the transdiagnostic PsyCourse Study, comprising patients of the affective-to-psychotic spectrum and controls, we investigated the genetic basis of the time course of two core executive subfunctions: set-shifting (Trail Making Test, part B (TMT-B)) and updating (Verbal Digit Span backwards) in 1338 genotyped individuals. Time course was assessed with four measurement points, each 6 months apart. Compared to the initial assessment, executive performance improved across diagnostic groups. We performed a genome-wide association study to identify single nucleotide polymorphisms (SNPs) associated with performance change over time by testing for SNP-by-time interactions using linear mixed models. We identified nine genome-wide significant SNPs for TMT-B in strong linkage disequilibrium with each other on chromosome 5. These were associated with decreased performance on the continuous TMT-B score across time. Variant rs150547358 had the lowest P value = 7.2 × 10 −10 with effect estimate beta = 1.16 (95% c.i.: 1.11, 1.22). Implementing data of the FOR2107 consortium (1795 individuals), we replicated these findings for the SNP rs150547358 ( P value = 0.015), analyzing the difference of the two available measurement points two years apart. In the replication study, rs150547358 exhibited a similar effect estimate beta = 0.85 (95% c.i.: 0.74, 0.97). Our study demonstrates that longitudinally measured phenotypes have the potential to unmask novel associations, adding time as a dimension to the effects of genomics."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41398-021-01510-8"],["dc.identifier.pii","1510"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88326"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2158-3188"],["dc.rights","CC BY 4.0"],["dc.title","A genome-wide association study of the longitudinal course of executive functions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Islam, Md Rezaul; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kaurani, Lalit; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Berulava, Tea; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Heilbronner, Urs; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Budde, Monika; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Centeno, Tonatiuh Pena; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Elerdashvili, Vakthang; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Zafieriou, Maria‐Patapia; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Benito, Eva; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sertel, Sinem M; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Goldberg, Maria; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Senner, Fanny; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Kalman, Janos L; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Burkhardt, Susanne; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Oepen, Anne Sophie; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sakib, Mohammad Sadman; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kerimoglu, Cemil; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Wirths, Oliver; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bickeböller, Heike; 7Department of Genetic Epidemiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bartels, Claudia; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Brosseron, Frederic; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Buerger, Katharina; 10German Center for Neurodegenerative Diseases (DZNE, Munich) Munich Germany"],["dc.contributor.affiliation","Cosma, Nicoleta‐Carmen; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Fliessbach, Klaus; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Heneka, Michael T.; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Janowitz, Daniel; 11Institute for Stroke and Dementia Research (ISD) University Hospital LMU Munich Munich Germany"],["dc.contributor.affiliation","Kilimann, Ingo; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Kleinedam, Luca; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Laske, Christoph; 14Department of Psychosomatic Medicine Rostock University Medical Center Rostock Germany"],["dc.contributor.affiliation","Metzger, Coraline D; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Munk, Matthias H; 15Section for Dementia Research Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy University of Tübingen Tübingen Germany"],["dc.contributor.affiliation","Perneczky, Robert; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Peters, Oliver; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Priller, Josef; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Rauchmann, Boris S.; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Roy, Nina; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Schneider, Anja; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spottke, Annika; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spruth, Eike J; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Teipel, Stefan; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Tscheuschler, Maike; 25Department of Psychiatry Medical Faculty University of Cologne Cologne Germany"],["dc.contributor.affiliation","Wagner, Michael; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Düzel, Emrah; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Jessen, Frank; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Rizzoli, Silvio O; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Zimmermann, Wolfram‐Hubertus; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Berulava, Tea"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Elerdashvili, Vakthang"],["dc.contributor.author","Zafieriou, Maria‐Patapia"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Sertel, Sinem M."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.authorgroup","Delcode Study Group"],["dc.date.accessioned","2021-12-01T09:24:01Z"],["dc.date.available","2021-12-01T09:24:01Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T13:34:49Z"],["dc.description.abstract","Abstract While some individuals age without pathological memory impairments, others develop age‐associated cognitive diseases. Since changes in cognitive function develop slowly over time in these patients, they are often diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. Thus, there is great need for the identification of inexpensive and minimal invasive approaches that could be used for screening with the aim to identify individuals at risk for cognitive decline that can then undergo further diagnostics and eventually stratified therapies. In this study, we use an integrative approach combining the analysis of human data and mechanistic studies in model systems to identify a circulating 3‐microRNA signature that reflects key processes linked to neural homeostasis and inform about cognitive status. We furthermore provide evidence that expression changes in this signature represent multiple mechanisms deregulated in the aging and diseased brain and are a suitable target for RNA therapeutics."],["dc.description.abstract","SYNOPSIS image Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. Circulating microRNAs are linked to cognitive function in young and healthy humans. A circulating 3‐microRNA signature is identified using a longitudinal mouse model of age‐associated memory decline. The expression of the 3‐microRNA signature is increased in patients with mild cognitive impairment (MCI) and is associated with future conversion from MCI to AD. Targeting all 3‐ microRNAs using anti‐miRs ameliorates cognitive decline in AD mice."],["dc.description.abstract","Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. image"],["dc.description.sponsorship","EC|H2020|H2020 Priority Excellent Science|H2020 European Research Council (ERC) http://dx.doi.org/10.13039/100010663"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung (BMBF) http://dx.doi.org/10.13039/501100002347"],["dc.description.sponsorship","HHS|NIH|OSC|Common Fund (NIH Common Fund) http://dx.doi.org/10.13039/100015326"],["dc.identifier.doi","10.15252/emmm.202013659"],["dc.identifier.pmid","34633146"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94824"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/411"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/150"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","A microRNA signature that correlates with cognition and is a target against cognitive decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","46276"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Neural plasticity"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Perez-Cruz, Claudia"],["dc.contributor.author","Müller-Keuker, Jeanine I. H."],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Flügge, Gabriele"],["dc.date.accessioned","2019-07-09T11:52:28Z"],["dc.date.available","2019-07-09T11:52:28Z"],["dc.date.issued","2007"],["dc.description.abstract","The prefrontal cortex (PFC) plays an important role in the stress response. We filled pyramidal neurons in PFC layer III with neurobiotin and analyzed dendrites in rats submitted to chronic restraint stress and in controls. In the right prelimbic cortex (PL) of controls, apical and distal dendrites were longer than in the left PL. Stress reduced the total length of apical dendrites in right PL and abolished the hemispheric difference. In right infralimbic cortex (IL) of controls, proximal apical dendrites were longer than in left IL, and stress eliminated this hemispheric difference. No hemispheric difference was detected in anterior cingulate cortex (ACx) of controls, but stress reduced apical dendritic length in left ACx. These data demonstrate interhemispheric differences in the morphology of pyramidal neurons in PL and IL of control rats and selective effects of stress on the right hemisphere. In contrast, stress reduced dendritic length in the left ACx."],["dc.identifier.doi","10.1155/2007/46276"],["dc.identifier.fs","207216"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4359"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60197"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1687-5443"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.ddc","599.8"],["dc.title","Morphology of Pyramidal Neurons in the Rat Prefrontal Cortex: Lateralized Dendritic Remodeling by Chronic Stress"],["dc.title.alternative","Research Article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0198249"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Flatau, Laura"],["dc.contributor.author","Reitt, Markus"],["dc.contributor.author","Duttge, Gunnar"],["dc.contributor.author","Lenk, Christian"],["dc.contributor.author","Zoll, Barbara"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Weber, Alexandra"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Kesberg, Rebekka"],["dc.contributor.author","Nagel, Jonas"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.editor","DeAngelis, Margaret M."],["dc.date.accessioned","2020-12-10T18:42:07Z"],["dc.date.available","2020-12-10T18:42:07Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1371/journal.pone.0198249"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15687"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77816"],["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","Genomic information and a person’s right not to know: A closer look at variations in hypothetical informational preferences in a German sample"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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","1"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Varbanov, Hristo"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Anghelescu, Ion"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Costa, Joan"],["dc.contributor.author","Medina, Juan"],["dc.contributor.author","Dietrich, Detlef E."],["dc.contributor.author","Figge, Christian"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Koller, Manfred"],["dc.contributor.author","Konrad, Carsten"],["dc.contributor.author","Nussbeck, Sara Y."],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Spitzer, Carsten"],["dc.contributor.author","Stierl, Sebastian"],["dc.contributor.author","Stöckel, Judith"],["dc.contributor.author","Thiel, Andreas"],["dc.contributor.author","von Hagen, Martin"],["dc.contributor.author","Zimmermann, Jörg"],["dc.contributor.author","Zitzelsberger, Antje"],["dc.contributor.author","Schulz, Sybille"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Dityatev, Alexander"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:44:03Z"],["dc.date.available","2018-01-09T14:44:03Z"],["dc.date.issued","2017-06-06"],["dc.description.abstract","Schizophrenia is a devastating disease that arises on the background of genetic predisposition and environmental risk factors, such as early life stress (ELS). In this study, we show that ELS-induced schizophrenia-like phenotypes in mice correlate with a widespread increase of histone-deacetylase 1 (Hdac1) expression that is linked to altered DNA methylation. Hdac1 overexpression in neurons of the medial prefrontal cortex, but not in the dorsal or ventral hippocampus, mimics schizophrenia-like phenotypes induced by ELS. Systemic administration of an HDAC inhibitor rescues the detrimental effects of ELS when applied after the manifestation of disease phenotypes. In addition to the hippocampus and prefrontal cortex, mice subjected to ELS exhibit increased Hdac1 expression in blood. Moreover, Hdac1 levels are increased in blood samples from patients with schizophrenia who had encountered ELS, compared with patients without ELS experience. Our data suggest that HDAC1 inhibition should be considered as a therapeutic approach to treat schizophrenia."],["dc.identifier.doi","10.1073/pnas.1613842114"],["dc.identifier.pmid","28533418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11605"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1091-6490"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 links early life stress to schizophrenia-like phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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"]]