Schulze, Thomas Gerd

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","209"],["dc.contributor.author","Kalman, Janos L."],["dc.contributor.author","Bresnahan, Michaeline"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Susser, Ezra"],["dc.date.accessioned","2020-12-10T15:21:11Z"],["dc.date.available","2020-12-10T15:21:11Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.schres.2019.05.012"],["dc.identifier.issn","0920-9964"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72940"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Predictors of persisting psychotic like experiences in children and adolescents: A scoping review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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","1123"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","International Archives of Occupational and Environmental Health"],["dc.bibliographiccitation.lastpage","1131"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Heutelbeck, Astrid R. R."],["dc.contributor.author","Junghans, Carsten"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Hallier, Ernst"],["dc.contributor.author","Schulz, Thomas G."],["dc.date.accessioned","2018-11-07T11:23:45Z"],["dc.date.available","2018-11-07T11:23:45Z"],["dc.date.issued","2009"],["dc.description.abstract","Introduction Cattle are an important source of allergens in the working area of farmers. Asthma caused by cow allergens is a significant occupational problem. Yet in allergological testing, the results of in vivo and in vitro diagnostic tests are often inconsistent even in cases with clearly cattle-related symptoms. Objectives and methods The aim of this study was to investigate four different commercial cow allergen extracts and to compare them with self prepared extracts of different cattle breeds by means of SDS-PAGE and immunoblotting using the sera of 42 German farmers with asthma and rhino-conjunctivitis caused by cattle contact. Results The commercial extracts investigated in this study showed only minor differences in protein pattern. Using sera in immunoblotting experiments distinct bands were found for all symptomatic farmers, even in 13 farmers with a negative result in commercially available serological allergy tests. Bands with molecular weights in the range between about 11 and 67 kDa were observed; reactivity with the major allergen Bos d 2 at about 20 kDa was detected in all farmers, although it was not the strongest band in all cases. Conclusions We demonstrate for the first time the allergenic relevance of additional proteins with molecular weights of 14, 30, 55 and approx. 67-97 kDa in more than 50% of farmers with cattle related symptoms. One of our most striking results was that 32% of the investigated farmers with cattle related symptoms showed negative results with commercial serological tests but distinct reactions with cow allergen in immunoblotting experiments. The Bos d 2 content in hair showed differences between certain breeds whereas German Brown and Simmental had particularly higher quantities of Bos d 2 in their hair than breeds such as Holstein-Friesian. These results strongly support the following recommendation: test results with commercial extracts that are contradictory to the clinical symptoms should be supplemented by skin tests using extracts of the hair of the farmers' own cattle."],["dc.identifier.doi","10.1007/s00420-009-0400-2"],["dc.identifier.isi","000270736700009"],["dc.identifier.pmid","19238424"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56255"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-0131"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Exposure to allergens of different cattle breeds and their relevance in occupational allergy"],["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.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Reinbold, Céline S."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Hecker, Julian"],["dc.contributor.author","Fullerton, Janice M."],["dc.contributor.author","Hoffmann, Per"],["dc.contributor.author","Hou, Liping"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Adli, Mazda"],["dc.contributor.author","Akiyama, Kazufumi"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2020-12-10T18:46:52Z"],["dc.date.available","2020-12-10T18:46:52Z"],["dc.date.issued","2018"],["dc.description.abstract","Bipolar disorder (BD) is a common, highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. Lithium is the best-established long-term treatment for BD, even though individual response is highly variable. Evidence suggests that some of this variability has a genetic basis. This is supported by the largest genome-wide association study (GWAS) of lithium response to date conducted by the International Consortium on Lithium Genetics (ConLiGen). Recently, we performed the first genome-wide analysis of the involvement of miRNAs in BD and identified nine BD-associated miRNAs. However, it is unknown whether these miRNAs are also associated with lithium response in BD. In the present study, we therefore tested whether common variants at these nine candidate miRNAs contribute to the variance in lithium response in BD. Furthermore, we systematically analyzed whether any other miRNA in the genome is implicated in the response to lithium. For this purpose, we performed gene-based tests for all known miRNA coding genes in the ConLiGen GWAS dataset (n = 2,563 patients) using a set-based testing approach adapted from the versatile gene-based test for GWAS (VEGAS2). In the candidate approach, miR-499a showed a nominally significant association with lithium response, providing some evidence for involvement in both development and treatment of BD. In the genome-wide miRNA analysis, 71 miRNAs showed nominally significant associations with the dichotomous phenotype and 106 with the continuous trait for treatment response. A total of 15 miRNAs revealed nominal significance in both phenotypes with miR-633 showing the strongest association with the continuous trait (p = 9.80E-04) and miR-607 with the dichotomous phenotype (p = 5.79E-04). No association between miRNAs and treatment response to lithium in BD in either of the tested conditions withstood multiple testing correction. Given the limited power of our study, the investigation of miRNAs in larger GWAS samples of BD and lithium response is warranted."],["dc.identifier.doi","10.3389/fpsyt.2018.00207"],["dc.identifier.eissn","1664-0640"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78571"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Analysis of the Influence of microRNAs in Lithium Response in Bipolar Disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1002134"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Smith, Erin N."],["dc.contributor.author","Koller, Daniel L."],["dc.contributor.author","Panganiban, Corrie"],["dc.contributor.author","Szelinger, Szabolcs"],["dc.contributor.author","Zhang, P."],["dc.contributor.author","Badner, Judith A."],["dc.contributor.author","Barrett, Thomas B."],["dc.contributor.author","Berrettini, Wade H."],["dc.contributor.author","Bloss, Cinnamon S."],["dc.contributor.author","Byerley, William"],["dc.contributor.author","Coryell, William"],["dc.contributor.author","Edenberg, Howard J."],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Gershon, Elliot S."],["dc.contributor.author","Greenwood, Tiffany A."],["dc.contributor.author","Guo, Yiran"],["dc.contributor.author","Hipolito, Maria"],["dc.contributor.author","Keating, Brendan J."],["dc.contributor.author","Lawson, William B."],["dc.contributor.author","Liu, Chunyu"],["dc.contributor.author","Mahon, Pamela Belmonte"],["dc.contributor.author","McInnis, Melvin G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","McKinney, Rebecca"],["dc.contributor.author","Murray, Sarah S."],["dc.contributor.author","Nievergelt, Caroline M."],["dc.contributor.author","Nurnberger, John I., Jr."],["dc.contributor.author","Nwulia, Evaristus A."],["dc.contributor.author","Potash, James B."],["dc.contributor.author","Rice, John"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Scheftner, William A."],["dc.contributor.author","Shilling, Paul D."],["dc.contributor.author","Zandi, Peter P."],["dc.contributor.author","Zoellner, Sebastian"],["dc.contributor.author","Craig, David W."],["dc.contributor.author","Schork, Nicholas J."],["dc.contributor.author","Kelsoe, John R."],["dc.date.accessioned","2018-11-07T08:55:17Z"],["dc.date.available","2018-11-07T08:55:17Z"],["dc.date.issued","2011"],["dc.description.abstract","Although a highly heritable and disabling disease, bipolar disorder's (BD) genetic variants have been challenging to identify. We present new genotype data for 1,190 cases and 401 controls and perform a genome-wide association study including additional samples for a total of 2,191 cases and 1,434 controls. We do not detect genome-wide significant associations for individual loci; however, across all SNPs, we show an association between the power to detect effects calculated from a previous genome-wide association study and evidence for replication (P = 1.5 x 10(-7)). To demonstrate that this result is not likely to be a false positive, we analyze replication rates in a large meta-analysis of height and show that, in a large enough study, associations replicate as a function of power, approaching a linear relationship. Within BD, SNPs near exons exhibit a greater probability of replication, supporting an enrichment of reproducible associations near functional regions of genes. These results indicate that there is likely common genetic variation associated with BD near exons (+/- 10 kb) that could be identified in larger studies and, further, provide a framework for assessing the potential for replication when combining results from multiple studies."],["dc.identifier.doi","10.1371/journal.pgen.1002134"],["dc.identifier.isi","000292386300049"],["dc.identifier.pmid","21738484"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22870"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7390"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Genome-Wide Association of Bipolar Disorder Suggests an Enrichment of Replicable Associations in Regions near Genes"],["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.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Popovic, David"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Senner, Fanny"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Koutsouleris, Nikolaos"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Fischer, André"],["dc.date.accessioned","2020-12-10T18:44:34Z"],["dc.date.available","2020-12-10T18:44:34Z"],["dc.date.issued","2019"],["dc.description.abstract","Schizophrenia is a severe neuropsychiatric disorder with persistence of symptoms throughout adult life in most of the affected patients. This unfavorable course is associated with multiple episodes and residual symptoms, mainly negative symptoms and cognitive deficits. The neural diathesis-stress model proposes that psychosocial stress acts on a pre-existing vulnerability and thus triggers the symptoms of schizophrenia. Childhood trauma is a severe form of stress that renders individuals more vulnerable to developing schizophrenia; neurobiological effects of such trauma on the endocrine system and epigenetic mechanisms are discussed. Childhood trauma is associated with impaired working memory, executive function, verbal learning, and attention in schizophrenia patients, including those at ultra-high risk to develop psychosis. In these patients, higher levels of childhood trauma were correlated with higher levels of attenuated positive symptoms, general symptoms, and depressive symptoms; lower levels of global functioning; and poorer cognitive performance in visual episodic memory end executive functions. In this review, we discuss effects of specific gene variants that interact with childhood trauma in patients with schizophrenia and describe new findings on the brain structural and functional level. Additive effects between childhood trauma and brain-derived neurotrophic factor methionine carriers on volume loss of the hippocampal subregions cornu ammonis (CA)4/dentate gyrus and CA2/3 have been reported in schizophrenia patients. A functional magnetic resonance imaging study showed that childhood trauma exposure resulted in aberrant function of parietal areas involved in working memory and of visual cortical areas involved in attention. In a theory of mind task reflecting social cognition, childhood trauma was associated with activation of the posterior cingulate gyrus, precuneus, and dorsomedial prefrontal cortex in patients with schizophrenia. In addition, decreased connectivity was shown between the posterior cingulate/precuneus region and the amygdala in patients with high levels of physical neglect and sexual abuse during childhood, suggesting that disturbances in specific brain networks underlie cognitive abilities. Finally, we discuss some of the questionnaires that are commonly used to assess childhood trauma and outline possibilities to use recent biostatistical methods, such as machine learning, to analyze the resulting datasets."],["dc.identifier.doi","10.3389/fnins.2019.00274"],["dc.identifier.eissn","1662-453X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78509"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-453X"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Childhood Trauma in Schizophrenia: Current Findings and Research Perspectives"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.issue","1"],["dc.bibliographiccitation.journal","International Journal of Bipolar Disorders"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Ritter, Philipp S."],["dc.contributor.author","Bermpohl, Felix"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Hautzinger, Martin"],["dc.contributor.author","Jansen, Andreas"],["dc.contributor.author","Juckel, Georg"],["dc.contributor.author","Kircher, Tilo"],["dc.contributor.author","Lambert, Martin"],["dc.contributor.author","Mulert, Christoph"],["dc.contributor.author","Pfennig, Andrea"],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Rienhoff, Otto"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Severus, Emanuel"],["dc.contributor.author","Stamm, Thomas"],["dc.contributor.author","Bauer, Michael"],["dc.date.accessioned","2019-07-09T11:43:13Z"],["dc.date.available","2019-07-09T11:43:13Z"],["dc.date.issued","2016"],["dc.description.abstract","Background Bipolar disorder is a severe and heterogeneous mental disorder. Despite great advances in neuroscience over the past decades, the precise causative mechanisms at the transmitter, cellular or network level have so far not been unraveled. As a result, individual treatment decisions cannot be tailor-made and the uncertain prognosis is based on clinical characteristics alone. Although a subpopulation of patients have an excellent response to pharmacological monotherapy, other subpopulations have been less well served by the medical system and therefore require more focused attention. In particular individuals at high risk of bipolar disorder, young patients in the early stages of bipolar disorder, patients with an unstable highly relapsing course and patients with acute suicidal ideation have been identified as those in need. Structure A research consortium of ten universities across Germany has therefore implemented a 4 year research agenda including three randomized controlled trials, one epidemiological trial and one cross-sectional trial to address these areas of unmet needs. The topics under investigation will be the improvement of early recognition, specific psychotherapy, and smartphones as an aid for early episode detection and biomarkers of lithium response. A subset of patients will be investigated utilizing neuroimaging (fMRI), neurophysiology (EEG), and biomaterials (genomics, transcriptomics). Conclusions This article aims to outline the rationale, design, and methods of these individual studies."],["dc.identifier.doi","10.1186/s40345-016-0066-0"],["dc.identifier.pmid","27873290"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58843"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2194-7511"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Aims and structure of the German Research Consortium BipoLife for the study of bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]