Schulze, Thomas Gerd

[["dc.bibliographiccitation.artnumber","e165"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Vassos, Evangelos"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Josef, F."],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Mueller-Myhsok, Bertram"],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Schmael, C."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Noethen, M. M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2018-11-07T09:06:00Z"],["dc.date.available","2018-11-07T09:06:00Z"],["dc.date.issued","2012"],["dc.description.abstract","Research suggests that clinical symptom dimensions may be more useful in delineating the genetics of bipolar disorder (BD) than standard diagnostic models. To date, no study has applied this concept to data from genome-wide association studies (GWAS). We performed a GWAS of factor dimensions in 927 clinically well-characterized BD patients of German ancestry. Rs9875793, which is located in an intergenic region of 3q26.1 and in the vicinity of the solute carrier family 2 (facilitated glucose transporter), member 2 gene (SLC2A2), was significantly associated with the factor analysis-derived dimension 'negative mood delusions' (n = 927; P = 4.65 x 10(-8), odds ratio (OR) = 2.66). This dimension was comprised of the symptoms delusions of poverty, delusions of guilt and nihilistic delusions. In case-control analyses, significant association with the G allele of rs9875793 was only observed in the subgroup of BD patients who displayed symptoms of 'negative mood delusions' (allelic chi(2) model: P-G = 0.0001, OR = 1.92; item present, n = 89). Further support for the hypothesis that rs9875793 is associated with BD in patients displaying 'negative mood delusions' symptom, such as delusions of guilt, was obtained from an European American sample (GAIN/TGEN), which included 1247 BD patients and 1434 controls (P-EA = 0.028, OR = 1.27). Translational Psychiatry (2012) 2, e165; doi:10.1038/tp.2012.81; published online 25 September 2012"],["dc.identifier.doi","10.1038/tp.2012.81"],["dc.identifier.isi","000312900000008"],["dc.identifier.pmid","23010768"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25455"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2158-3188"],["dc.title","Genome-wide significant association between a 'negative mood delusions' dimension in bipolar disorder and genetic variation on chromosome 3q26.1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Alcohol"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Hothorn, Ludwig A."],["dc.contributor.author","Schaarschmidt, Frank"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Stuermer, Til"],["dc.contributor.author","Amelang, Manfred"],["dc.contributor.author","Zhu, G. U."],["dc.contributor.author","Whitfield, John B."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","de Moor, Marleen H. M."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2018-11-07T09:43:07Z"],["dc.date.available","2018-11-07T09:43:07Z"],["dc.date.issued","2014"],["dc.format.extent","191"],["dc.identifier.isi","000333505000132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34106"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","Conference on Alcoholism and Stress - A Framework for Future Treatment Strategies"],["dc.relation.eventlocation","Volterra, ITALY"],["dc.relation.issn","1873-6823"],["dc.relation.issn","0741-8329"],["dc.title","Association and replication study of NPY2R promoter variant rs6857715 with drinking and smoking behavior in patients and the general population"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.firstpage","S395"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","S396"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Andlauer, Till F.M."],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Kalman, Janos"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Nöthen, Markus"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Witt, Stephanie"],["dc.contributor.author","Müller-Myhsok, Bertram"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2020-12-10T14:23:51Z"],["dc.date.available","2020-12-10T14:23:51Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.euroneuro.2016.09.433"],["dc.identifier.issn","0924-977X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72065"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Using Polygenic Scores Based on Schneiderian First Rank Symptoms To Characterize Disease Trajectories In Severe Mental Illnesses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The American Journal of Human Genetics"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Miro, Xavier"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Meesters, Christian"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Weingarten, Moritz"],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Alexander, Michael J."],["dc.contributor.author","Vollmer, Jennifer"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Tessmann, Peter"],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Schreiber, Stefan"],["dc.contributor.author","Mueller-Myhsok, Bertram"],["dc.contributor.author","Lucae, Susanne"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Leboyer, Marion"],["dc.contributor.author","Bellivier, Frank"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Kahn, Jean-Pierre"],["dc.contributor.author","Heath, Simon"],["dc.contributor.author","Hamshere, Marian L."],["dc.contributor.author","O'Donovan, Michael C."],["dc.contributor.author","Owen, Michael J."],["dc.contributor.author","Craddock, Nick"],["dc.contributor.author","Schwarz, Markus"],["dc.contributor.author","Vedder, Helmut"],["dc.contributor.author","Kammerer-Ciernioch, Jutta"],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Sasse, Johanna"],["dc.contributor.author","Bauer, Michael"],["dc.contributor.author","Hautzinger, Martin"],["dc.contributor.author","Wright, Adam"],["dc.contributor.author","Mitchell, Philip B."],["dc.contributor.author","Schofield, Peter R."],["dc.contributor.author","Montgomery, Grant W."],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Gordon, Scott D."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Gustafsson, Omar"],["dc.contributor.author","Andreassen, Ole A."],["dc.contributor.author","Djurovic, Srdjan"],["dc.contributor.author","Sigurdsson, Engilbert"],["dc.contributor.author","Steinberg, Stacy"],["dc.contributor.author","Stefansson, Hreinn"],["dc.contributor.author","Stefansson, Kari"],["dc.contributor.author","Kapur-Pojskic, Lejla"],["dc.contributor.author","Oruc, Liliana"],["dc.contributor.author","Rivas, Fabio"],["dc.contributor.author","Mayoral, Fermin"],["dc.contributor.author","Chuchalin, Alexander"],["dc.contributor.author","Babadjanova, Gulja"],["dc.contributor.author","Tiganov, Alexander S."],["dc.contributor.author","Pantelejeva, Galina"],["dc.contributor.author","Abramova, Lilia I."],["dc.contributor.author","Grigoroiu-Serbanescu, Maria"],["dc.contributor.author","Diaconu, Carmen C."],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Zimmer, Andreas"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Noethen, Markus M."],["dc.date.accessioned","2018-11-07T08:58:10Z"],["dc.date.available","2018-11-07T08:58:10Z"],["dc.date.issued","2011"],["dc.format.extent","396"],["dc.identifier.doi","10.1016/j.ajhg.2011.03.001"],["dc.identifier.isi","000288589000019"],["dc.identifier.pmid","21353194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0002-9297"],["dc.title","Genome-wide Association Study Identifies Genetic Variation in Neurocan as a Susceptibility Factor for Bipolar Disorder (vol 88, pg 372, 2011)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","24"],["dc.bibliographiccitation.issue","1-3"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","30"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Nieratschker, Vanessa"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Wendland, Jens R."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Abou Jamra, Rami"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2018-11-07T08:40:11Z"],["dc.date.available","2018-11-07T08:40:11Z"],["dc.date.issued","2010"],["dc.description.abstract","The aim of the present study was to investigate possible associations between schizophrenia and 13 SNP markers in COMT. No association was observed in 631 cases, 207 nuclear families, and 776 controls. A cognitive performance phenotype (Trail Marking Test) was available for a subgroup of the patients. No association was found between the 13 markers and this phenotype. Four clinically-defined subgroups (early age at onset, negative symptoms, family history of schizophrenia, and life-time major depressive episode) were also investigated. Associations were observed for 3 of these subgroups, although none withstood correction for multiple testing. COMT does not appear to be a risk factor for schizophrenia in this population. (C) 2010 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.schres.2010.06.018"],["dc.identifier.isi","000286406900002"],["dc.identifier.pmid","20643532"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19164"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0920-9964"],["dc.title","The catechol-O-methyl transferase (COMT) gene and its potential association with schizophrenia: Findings from a large German case-control and family-based sample"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","607"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","613"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Amelang, Manfred"],["dc.contributor.author","Hothorn, Ludwig A."],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Nieratschker, V."],["dc.contributor.author","Gerhard, Daniel"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Wuest, S."],["dc.contributor.author","Frank, J."],["dc.contributor.author","Loerbroks, Adrian"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Stuermer, Til"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2018-11-07T09:25:24Z"],["dc.date.available","2018-11-07T09:25:24Z"],["dc.date.issued","2013"],["dc.description.abstract","Genome-wide association studies have reported an association between the A-allele of rs1006737 within CACNA1C and affective disorders and schizophrenia. The aim of the present study was to investigate the relationship between rs1006737 and established and potential endophenotypes for these disorders in a population-based cohort of 3793 subjects, using an analytical method designed to assess a previously reported sex-specific effect of CACNA1C. The investigated endophenotypes included personality traits and resilience factors. At 10-year follow-up, subjects were screened for depressive symptoms. All subjects were genotyped for rs1006737. The direction of the effect and mode of inheritance of rs1006737 differed between the sexes. In men, the A-allele was associated with higher emotional lability and lower resilience, that is, lower sense of coherence (P = 0.021), lower perceived social support (P = 0.018), lower dispositional optimism (P = 0.032) and more depressive symptoms at follow-up (P = 0.007). In women, the A-allele was associated with lower emotional lability and stronger resilience, that is, higher sense of coherence (P = 0.00028), higher perceived social support (P = 0.010), lower neuroticism (P = 0.022) and fewer depressive symptoms at follow-up (P = 0.035). After conservative Bonferroni correction for 32 tests, results only remained significant for sense of coherence in women (P = 0.009). These results suggest that CACNA1C is involved in the genetic architecture of endophenotypes for affective disorders and schizophrenia, and that it shows a distinct sex-specific effect. Comprehensive phenotype characterization in case-control samples and the general population, as well as an adequate modeling of sex-specific genetic effects, may be warranted to elucidate the pathogenetic mechanisms conferred by robustly identified susceptibility genes. Molecular Psychiatry (2013) 18, 607-613; doi:10.1038/mp.2012.53; published online 5 June 2012"],["dc.identifier.doi","10.1038/mp.2012.53"],["dc.identifier.isi","000317952700012"],["dc.identifier.pmid","22665259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30057"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","The psychiatric vulnerability gene CACNA1C and its sex-specific relationship with personality traits, resilience factors and depressive symptoms in the general population"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","237"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","248"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Gade, Katrin"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Anderson-Schmidt, Heike"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2018-11-07T09:56:47Z"],["dc.date.available","2018-11-07T09:56:47Z"],["dc.date.issued","2015"],["dc.description.abstract","Objectives. Functional outcome has recently become of interest for cross-diagnostic subphenotype approaches in psychiatric genetics. Therefore, it is crucial to know about clinical, demographic and psychosocial variables that correlate with long-term functioning. Unfortunately, there is a lack of studies that directly compare the importance of correlates for functional outcome between different disorders. Methods. Applying regression models to samples of patients with schizophrenia (SZ, n = 238), bipolar disorder (BD, n = 533) and major depressive disorder (MDD, n = 398), we compared the magnitude of association of potential correlates with functional outcome, measured by the Global Assessment of Functioning (GAF) score. Results. Shared correlates for worse functional outcome were poor premorbid functioning, insidious illness onset and poor premorbid work or social adjustment in all three disorders, and negative symptomatology in SZ and BD. Disorder-specific correlates for SZ were longer duration of illness, lower functioning during episodes and being life-time single, for BD substance abuse and suicidality, and for MDD premorbid unemployment and having a premorbid personality disorder. Conclusions. We found different patterns of correlates for long-term functioning in SZ, BD and MDD. Knowledge of these patterns may improve the quality of genetic investigations focussing on functional outcome."],["dc.identifier.doi","10.3109/15622975.2014.995221"],["dc.identifier.isi","000354811400004"],["dc.identifier.pmid","25771936"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37032"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1814-1412"],["dc.relation.issn","1562-2975"],["dc.title","Functional outcome in major psychiatric disorders and associated clinical and psychosocial variables: A potential cross-diagnostic phenotype for further genetic investigations?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","906"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","917"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Kirsch, Peter"],["dc.contributor.author","Esslinger, Christine"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Demontis, D."],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Strengman, E."],["dc.contributor.author","Schmael, C."],["dc.contributor.author","Mors, Ole"],["dc.contributor.author","Mortensen, Preben Bo"],["dc.contributor.author","Hougaard, D. M."],["dc.contributor.author","Orntoft, Torben F."],["dc.contributor.author","Kapelski, P."],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Basmanav, F. Buket U."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Hoffmann, P."],["dc.contributor.author","Meier, Sandra"],["dc.contributor.author","Nikitopoulos, J."],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Alexander, M."],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Wichmann, H-E"],["dc.contributor.author","Schreiber, S."],["dc.contributor.author","Rivandeneira, Fernando"],["dc.contributor.author","Hofman, Albert"],["dc.contributor.author","Uitterlinden, Andre G."],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Schumacher, J."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Cantor, R. M."],["dc.contributor.author","Erk, S."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Craddock, N."],["dc.contributor.author","Owen, M. J."],["dc.contributor.author","O'Donovan, M. C."],["dc.contributor.author","Borglum, Anders D."],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Walter, H."],["dc.contributor.author","Meyer-Lindenberg, Andreas"],["dc.contributor.author","Noethen, M. M."],["dc.contributor.author","Ophoff, Roel A."],["dc.contributor.author","Cichon, Sven"],["dc.date.accessioned","2018-11-07T09:06:48Z"],["dc.date.available","2018-11-07T09:06:48Z"],["dc.date.issued","2012"],["dc.description.abstract","Recent molecular studies have implicated common alleles of small to moderate effect and rare alleles with larger effect sizes in the genetic architecture of schizophrenia (SCZ). It is expected that the reliable detection of risk variants with very small effect sizes can only be achieved through the recruitment of very large samples of patients and controls (that is tens of thousands), or large, potentially more homogeneous samples that have been recruited from confined geographical areas using identical diagnostic criteria. Applying the latter strategy, we performed a genome-wide association study (GWAS) of 1169 clinically well characterized and ethnically homogeneous SCZ patients from a confined area of Western Europe (464 from Germany, 705 from The Netherlands) and 3714 ethnically matched controls (1272 and 2442, respectively). In a subsequent follow-up study of our top GWAS results, we included an additional 2569 SCZ patients and 4088 controls (from Germany, The Netherlands and Denmark). Genetic variation in a region on chromosome 11 that contains the candidate genes AMBRA1, DGKZ, CHRM4 and MDK was significantly associated with SCZ in the combined sample (n = 11 540; P = 3.89 x 10(-9), odds ratio (OR) = 1.25). This finding was replicated in 23 206 independent samples of European ancestry (P = 0.0029, OR= 1.11). In a subsequent imaging genetics study, healthy carriers of the risk allele exhibited altered activation in the cingulate cortex during a cognitive control task. The area of interest is a critical interface between emotion regulation and cognition that is structurally and functionally abnormal in SCZ and bipolar disorder. Molecular Psychiatry (2012) 17, 906-917; doi: 10.1038/mp.2011.80; published online 12 July 2011"],["dc.identifier.doi","10.1038/mp.2011.80"],["dc.identifier.isi","000308063900007"],["dc.identifier.pmid","21747397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25636"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.title","Association between genetic variation in a region on chromosome 11 and schizophrenia in large samples from Europe"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]