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","e104326"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Georgi, Alexander"],["dc.contributor.author","Zidane, Nora"],["dc.contributor.author","Chevallier, Lucie"],["dc.contributor.author","Deshommes, Jasmine"],["dc.contributor.author","Nicolas, Aude"],["dc.contributor.author","Henrion, Annabelle"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Mathieu, Flavie"],["dc.contributor.author","Kahn, Jean-Pierre"],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Boland, Anne"],["dc.contributor.author","Zelenika, Diana"],["dc.contributor.author","Gut, Ivo"],["dc.contributor.author","Heath, Simon"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Albus, Margot"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Hamshere, Marian L."],["dc.contributor.author","Craddock, Nicholas"],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Bellivier, Frank"],["dc.contributor.author","Leboyer, Marion"],["dc.date.accessioned","2018-11-07T09:36:39Z"],["dc.date.available","2018-11-07T09:36:39Z"],["dc.date.issued","2014"],["dc.description.abstract","Bipolar disorder is one of the most common and devastating psychiatric disorders whose mechanisms remain largely unknown. Despite a strong genetic contribution demonstrated by twin and adoption studies, a polygenic background influences this multifactorial and heterogeneous psychiatric disorder. To identify susceptibility genes on a severe and more familial sub-form of the disease, we conducted a genome-wide association study focused on 211 patients of French origin with an early age at onset and 1,719 controls, and then replicated our data on a German sample of 159 patients with early-onset bipolar disorder and 998 controls. Replication study and subsequent meta-analysis revealed two genes encoding proteins involved in phosphoinositide signalling pathway (PLEKHA5 and PLCXD3). We performed additional replication studies in two datasets from the WTCCC (764 patients and 2,938 controls) and the GAIN-TGen cohorts (1,524 patients and 1,436 controls) and found nominal P-values both in the PLCXD3 and PLEKHA5 loci with the WTCCC sample. In addition, we identified in the French cohort one affected individual with a deletion at the PLCXD3 locus and another one carrying a missense variation in PLCXD3 (p.R93H), both supporting a role of the phosphatidylinositol pathway in early-onset bipolar disorder vulnerability. Although the current nominally significant findings should be interpreted with caution and need replication in independent cohorts, this study supports the strategy to combine genetic approaches to determine the molecular mechanisms underlying bipolar disorder."],["dc.identifier.doi","10.1371/journal.pone.0104326"],["dc.identifier.isi","000341105100048"],["dc.identifier.pmid","25111785"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32665"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Common and Rare Variant Analysis in Early-Onset Bipolar Disorder Vulnerability"],["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.artnumber","e38828"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Gladwin, Thomas E."],["dc.contributor.author","Derks, Eske M."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Levinson, Douglas"],["dc.contributor.author","Shi, Jianxin"],["dc.contributor.author","Gejman, Pablo V."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Ophoff, Roel A."],["dc.date.accessioned","2018-11-07T09:09:13Z"],["dc.date.available","2018-11-07T09:09:13Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent studies suggest that variation in complex disorders (e.g., schizophrenia) is explained by a large number of genetic variants with small effect size (Odds Ratio similar to 1.05-1.1). The statistical power to detect these genetic variants in Genome Wide Association (GWA) studies with large numbers of cases and controls (similar to 15,000) is still low. As it will be difficult to further increase sample size, we decided to explore an alternative method for analyzing GWA data in a study of schizophrenia, dramatically reducing the number of statistical tests. The underlying hypothesis was that at least some of the genetic variants related to a common outcome are collocated in segments of chromosomes at a wider scale than single genes. Our approach was therefore to study the association between relatively large segments of DNA and disease status. An association test was performed for each SNP and the number of nominally significant tests in a segment was counted. We then performed a permutation-based binomial test to determine whether this region contained significantly more nominally significant SNPs than expected under the null hypothesis of no association, taking linkage into account. Genome Wide Association data of three independent schizophrenia case/control cohorts with European ancestry (Dutch, German, and US) using segments of DNA with variable length (2 to 32 Mbp) was analyzed. Using this approach we identified a region at chromosome 5q23.3-q31.3 (128-160 Mbp) that was significantly enriched with nominally associated SNPs in three independent case-control samples. We conclude that considering relatively wide segments of chromosomes may reveal reliable relationships between the genome and schizophrenia, suggesting novel methodological possibilities as well as raising theoretical questions."],["dc.identifier.doi","10.1371/journal.pone.0038828"],["dc.identifier.isi","000305583300057"],["dc.identifier.pmid","22723893"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7934"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26207"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Segment-Wise Genome-Wide Association Analysis Identifies a Candidate Region Associated with Schizophrenia in Three Independent Samples"],["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","15351"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Rietschel, Liz"],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Zhu, Gu"],["dc.contributor.author","McAloney, Kerrie"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Couvy-Duchesne, Baptiste"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Binz, Tina M."],["dc.contributor.author","McGrath, John"],["dc.contributor.author","Hickie, Ian B."],["dc.contributor.author","Hansell, Narelle K."],["dc.contributor.author","Wright, Margaret J."],["dc.contributor.author","Gillespie, Nathan A."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Wüst, Stefan"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Baumgartner, Markus R."],["dc.contributor.author","Walker, Brian R."],["dc.contributor.author","Crawford, Andrew A."],["dc.contributor.author","Colodro-Conde, Lucía"],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2019-07-09T11:44:40Z"],["dc.date.available","2019-07-09T11:44:40Z"],["dc.date.issued","2017-11-10"],["dc.description.abstract","Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables."],["dc.identifier.doi","10.1038/s41598-017-11852-3"],["dc.identifier.pmid","29127340"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14860"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59064"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Hair Cortisol in Twins: Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes."],["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","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"]]