Schulze, Thomas Gerd

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","556"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Wuest, Stefan"],["dc.date.accessioned","2018-11-07T09:26:54Z"],["dc.date.available","2018-11-07T09:26:54Z"],["dc.date.issued","2013"],["dc.description.abstract","Linkage and fine mapping studies have established that the neuregulin 3 gene (NRG3) is a susceptibility locus for schizophrenia. Association studies of this disorder have implicated NRG3 variants in both psychotic symptoms and attention performance. Psychotic symptoms and cognitive deficits are also frequent features of bipolar disorder. The aims of the present study were to extend analysis of the association between NRG3 and psychotic symptoms and attention in schizophrenia and to determine whether these associations also apply to bipolar disorder. A total of 358 patients with schizophrenia and 111 patients with bipolar disorder were included. Psychotic symptoms were evaluated using the Operational Criteria Checklist for Psychotic Illness (OPCRIT) and attention performance was assessed using the Trail Making Test (TMT). Symptoms and performance scores were then tested for association with the NRG3 variant rs6584400. A significant association was found between the number of rs6584400 minor alleles and the total OPCRIT score for psychotic symptoms in patients with schizophrenia. Moreover, in both schizophrenia and bipolar disorder patients, minor allele carriers of rs6584400 outperformed homozygous major allele carriers in the TMT. The results suggest that rs6584400 is associated with psychotic symptoms and attention performance in schizophrenia. The finding of a significant association between rs6584400 and attention performance in bipolar disorder supports the hypothesis that this NRG3 variant confers genetic susceptibility to cognitive deficits in both schizophrenia and bipolar disorder."],["dc.identifier.doi","10.1017/S1461145712000697"],["dc.identifier.isi","000315527600006"],["dc.identifier.pmid","22831755"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10204"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30409"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1469-5111"],["dc.relation.issn","1461-1457"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Neuregulin 3 is associated with attention deficits in schizophrenia and 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.artnumber","24"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Bipolar Disorders"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Breuer, René"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Krumm, Bertram"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Kassem, Layla"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Mühleisen, Thomas W."],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Karypis, George"],["dc.contributor.author","Kelsoe, John"],["dc.contributor.author","Greenwood, Tiffany"],["dc.contributor.author","Nievergelt, Caroline"],["dc.contributor.author","Shilling, Paul"],["dc.contributor.author","Shekhtman, Tatyana"],["dc.contributor.author","Edenberg, Howard"],["dc.contributor.author","Craig, David"],["dc.contributor.author","Szelinger, Szabolcs"],["dc.contributor.author","Nurnberger, John"],["dc.contributor.author","Gershon, Elliot"],["dc.contributor.author","Alliey-Rodriguez, Ney"],["dc.contributor.author","Zandi, Peter"],["dc.contributor.author","Goes, Fernando"],["dc.contributor.author","Schork, Nicholas"],["dc.contributor.author","Smith, Erin"],["dc.contributor.author","Koller, Daniel"],["dc.contributor.author","Zhang, Peng"],["dc.contributor.author","Badner, Judith"],["dc.contributor.author","Berrettini, Wade"],["dc.contributor.author","Bloss, Cinnamon"],["dc.contributor.author","Byerley, William"],["dc.contributor.author","Coryell, William"],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Guo, Yirin"],["dc.contributor.author","Hipolito, Maria"],["dc.contributor.author","Keating, Brendan"],["dc.contributor.author","Lawson, William"],["dc.contributor.author","Liu, Chunyu"],["dc.contributor.author","Mahon, Pamela"],["dc.contributor.author","McInnis, Melvin"],["dc.contributor.author","Murray, Sarah"],["dc.contributor.author","Nwulia, Evaristus"],["dc.contributor.author","Potash, James"],["dc.contributor.author","Rice, John"],["dc.contributor.author","Scheftner, William"],["dc.contributor.author","Zöllner, Sebastian"],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2019-07-09T11:46:03Z"],["dc.date.available","2019-07-09T11:46:03Z"],["dc.date.issued","2018"],["dc.description.abstract","Background Disentangling the etiology of common, complex diseases is a major challenge in genetic research. For bipolar disorder (BD), several genome-wide association studies (GWAS) have been performed. Similar to other complex disorders, major breakthroughs in explaining the high heritability of BD through GWAS have remained elusive. To overcome this dilemma, genetic research into BD, has embraced a variety of strategies such as the formation of large consortia to increase sample size and sequencing approaches. Here we advocate a complementary approach making use of already existing GWAS data: a novel data mining procedure to identify yet undetected genotype–phenotype relationships. We adapted association rule mining, a data mining technique traditionally used in retail market research, to identify frequent and characteristic genotype patterns showing strong associations to phenotype clusters. We applied this strategy to three independent GWAS datasets from 2835 phenotypically characterized patients with BD. In a discovery step, 20,882 candidate association rules were extracted. Results Two of these rules—one associated with eating disorder and the other with anxiety—remained significant in an independent dataset after robust correction for multiple testing. Both showed considerable effect sizes (odds ratio ~ 3.4 and 3.0, respectively) and support previously reported molecular biological findings. Conclusion Our approach detected novel specific genotype–phenotype relationships in BD that were missed by standard analyses like GWAS. While we developed and applied our method within the context of BD gene discovery, it may facilitate identifying highly specific genotype–phenotype relationships in subsets of genome-wide data sets of other complex phenotype with similar epidemiological properties and challenges to gene discovery efforts."],["dc.identifier.doi","10.1186/s40345-018-0132-x"],["dc.identifier.pmid","30415424"],["dc.identifier.pmid","30415424"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15387"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59371"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Berlin"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/242257/EU/SGenomic variations underlying common behavior diseases and cognition trait in human populations/ADAMS"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Detecting significant genotype–phenotype association rules in bipolar disorder: market research meets complex genetics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","555"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics"],["dc.bibliographiccitation.lastpage","565"],["dc.bibliographiccitation.volume","180"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Lemme, Noemi"],["dc.contributor.author","Flatau, Laura"],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Foo, Jerome C."],["dc.contributor.author","Reitt, Markus"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Lanzerath, Dirk"],["dc.contributor.author","Illes, Franciska"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2020-12-10T14:07:19Z"],["dc.date.available","2020-12-10T14:07:19Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/ajmg.b.32724"],["dc.identifier.eissn","1552-485X"],["dc.identifier.issn","1552-4841"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16917"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70172"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Attitudes toward the right to autonomous decision‐making in psychiatric genetic testing: Controversial and context‐dependent"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e426"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Juraeva, Dilafruz"],["dc.contributor.author","Sticht, Carsten"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Dukal, H."],["dc.contributor.author","Frank, J."],["dc.contributor.author","Lang, M."],["dc.contributor.author","Deuschle, M."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Noethen, M. M."],["dc.contributor.author","Witt, C. C."],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2018-11-07T09:36:50Z"],["dc.date.available","2018-11-07T09:36:50Z"],["dc.date.issued","2014"],["dc.description.abstract","Bipolar disorder (BD) is a highly heritable psychiatric disease characterized by recurrent episodes of mania and depression. To identify new BD genes and pathways, the present study employed a three-step approach. First, gene-expression profiles of BD patients were assessed during both a manic and an euthymic phase. These profiles were compared intra-individually and with the gene-expression profiles of controls. Second, those differentially expressed genes that were considered potential trait markers of BD were validated using data from the Psychiatric Genomics Consortiums' genome-wide association study (GWAS) of BD. Third, the implicated molecular mechanisms were investigated using pathway analytical methods. In the present patients, this novel approach identified: (i) sets of differentially expressed genes specific to mania and euthymia; and (ii) a set of differentially expressed genes that were common to both mood states. In the GWAS data integration analysis, one gene (STAB1) remained significant (P = 1.9 x 10(-4)) after adjustment for multiple testing. STAB1 is located in close proximity to PBMR1 and the NEK4-ITIH1-ITIH3-ITIH4 region, which are the top findings from GWAS meta-analyses of mood disorder, and a combined BD and schizophrenia data set. Pathway analyses in the mania versus control comparison revealed three distinct clusters of pathways tagging molecular mechanisms implicated in BD, for example, energy metabolism, inflammation and the ubiquitin proteasome system. The present findings suggest that STAB1 is a new and highly promising candidate gene in this region. The combining of gene expression and GWAS data may provide valuable insights into the biological mechanisms of BD."],["dc.identifier.doi","10.1038/tp.2014.71"],["dc.identifier.isi","000344826900007"],["dc.identifier.pmid","25136889"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32704"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2158-3188"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Investigation of manic and euthymic episodes identifies state- and trait-specific gene expression and STAB1 as a new candidate gene for 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.artnumber","e1004345"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Juraeva, Dilafruz"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Zapatka, Marc"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Ripke, Stephan"],["dc.contributor.author","Leber, Markus"],["dc.contributor.author","Lange, Christoph"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Moessner, Rainald"],["dc.contributor.author","Nenadic, Igor"],["dc.contributor.author","Sauer, Heinrich"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Borglum, Anders D."],["dc.contributor.author","Ophoff, Roel A."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Noethen, MarkusM."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Brors, Benedikt"],["dc.date.accessioned","2018-11-07T09:39:10Z"],["dc.date.available","2018-11-07T09:39:10Z"],["dc.date.issued","2014"],["dc.description.abstract","In the present study, an integrated hierarchical approach was applied to: (1) identify pathways associated with susceptibility to schizophrenia; (2) detect genes that may be potentially affected in these pathways since they contain an associated polymorphism; and (3) annotate the functional consequences of such single-nucleotide polymorphisms (SNPs) in the affected genes or their regulatory regions. The Global Test was applied to detect schizophrenia-associated pathways using discovery and replication datasets comprising 5,040 and 5,082 individuals of European ancestry, respectively. Information concerning functional gene-sets was retrieved from the Kyoto Encyclopedia of Genes and Genomes, Gene Ontology, and the Molecular Signatures Database. Fourteen of the gene-sets or pathways identified in the discovery dataset were confirmed in the replication dataset. These include functional processes involved in transcriptional regulation and gene expression, synapse organization, cell adhesion, and apoptosis. For two genes, i.e. CTCF and CACNB2, evidence for association with schizophrenia was available (at the gene-level) in both the discovery study and published data from the Psychiatric Genomics Consortium schizophrenia study. Furthermore, these genes mapped to four of the 14 presently identified pathways. Several of the SNPs assigned to CTCF and CACNB2 have potential functional consequences, and a gene in close proximity to CACNB2, i.e. ARL5B, was identified as a potential gene of interest. Application of the present hierarchical approach thus allowed: (1) identification of novel biological gene-sets or pathways with potential involvement in the etiology of schizophrenia, as well as replication of these findings in an independent cohort; (2) detection of genes of interest for future follow-up studies; and (3) the highlighting of novel genes in previously reported candidate regions for schizophrenia."],["dc.identifier.doi","10.1371/journal.pgen.1004345"],["dc.identifier.isi","000338847700004"],["dc.identifier.pmid","24901509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10182"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33219"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.relation.issn","1553-7390"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Integrated Pathway-Based Approach Identifies Association between Genomic Regions at CTCF and CACNB2 and Schizophrenia"],["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.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","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.firstpage","156"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology : The Journal of the European College of Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Alliey-Rodriguez, Ney"],["dc.contributor.author","Ament, Seth"],["dc.contributor.author","Badner, Judith A."],["dc.contributor.author","Berrettini, Wade H."],["dc.contributor.author","Bloss, Cinnamon S."],["dc.contributor.author","Byerley, William"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Comes, Ashley L."],["dc.contributor.author","Coryell, William"],["dc.contributor.author","Craig, David W."],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Edenberg, Howard J."],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Gershon, Elliot S."],["dc.contributor.author","Goes, Fernando S."],["dc.contributor.author","Greenwood, Tiffany A."],["dc.contributor.author","Guo, Yiran"],["dc.contributor.author","Hipolito, Maria"],["dc.contributor.author","Hood, Leroy"],["dc.contributor.author","Keating, Brendan J."],["dc.contributor.author","Koller, Daniel L."],["dc.contributor.author","Lawson, William B."],["dc.contributor.author","Liu, Chunyu"],["dc.contributor.author","Mahon, Pamela B."],["dc.contributor.author","McInnis, Melvin G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Meier, Sandra M."],["dc.contributor.author","Mühleisen, Thomas W."],["dc.contributor.author","Murray, Sarah S."],["dc.contributor.author","Nievergelt, Caroline M."],["dc.contributor.author","Nurnberger, John I."],["dc.contributor.author","Nwulia, Evaristus A."],["dc.contributor.author","Potash, James B."],["dc.contributor.author","Quarless, Danjuma"],["dc.contributor.author","Rice, John"],["dc.contributor.author","Roach, Jared C."],["dc.contributor.author","Scheftner, William A."],["dc.contributor.author","Schork, Nicholas J."],["dc.contributor.author","Shekhtman, Tatyana"],["dc.contributor.author","Shilling, Paul D."],["dc.contributor.author","Smith, Erin N."],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Szelinger, Szabolcs"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Zandi, Peter P."],["dc.contributor.author","Zhang, Peng"],["dc.contributor.author","Zöllner, Sebastian"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Falkai, Peter G."],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Malzahn, Dörthe"],["dc.date.accessioned","2019-07-09T11:50:26Z"],["dc.date.available","2019-07-09T11:50:26Z"],["dc.date.issued","2019-"],["dc.description.abstract","Genome-wide association studies of case-control status have advanced the understanding of the genetic basis of psychiatric disorders. Further progress may be gained by increasing sample size but also by new analysis strategies that advance the exploitation of existing data, especially for clinically important quantitative phenotypes. The functionally-informed efficient region-based test strategy (FIERS) introduced herein uses prior knowledge on biological function and dependence of genotypes within a powerful statistical framework with improved sensitivity and specificity for detecting consistent genetic effects across studies. As proof of concept, FIERS was used for the first genome-wide single nucleotide polymorphism (SNP)-based investigation on bipolar disorder (BD) that focuses on an important aspect of disease course, the functional outcome. FIERS identified a significantly associated locus on chromosome 15 (hg38: chr15:48965004 - 49464789 bp) with consistent effect strength between two independent studies (GAIN/TGen: European Americans, BOMA: Germans; n = 1592 BD patients in total). Protective and risk haplotypes were found on the most strongly associated SNPs. They contain a CTCF binding site (rs586758); CTCF sites are known to regulate sets of genes within a chromatin domain. The rs586758 - rs2086256 - rs1904317 haplotype is located in the promoter flanking region of the COPS2 gene, close to microRNA4716, and the EID1, SHC4, DTWD1 genes as plausible biological candidates. While implication with BD is novel, COPS2, EID1, and SHC4 are known to be relevant for neuronal differentiation and function and DTWD1 for psychopharmacological side effects. The test strategy FIERS that enabled this discovery is equally applicable for tag SNPs and sequence data."],["dc.identifier.doi","10.1016/j.euroneuro.2018.10.005"],["dc.identifier.pmid","30503783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59772"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1873-7862"],["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","Efficient region-based test strategy uncovers genetic risk factors for functional outcome in bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]