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.firstpage","951"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","963"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Malhotra, Dheeraj"],["dc.contributor.author","McCarthy, Shane A."],["dc.contributor.author","Michaelson, Jacob J."],["dc.contributor.author","Vacic, Vladimir"],["dc.contributor.author","Burdick, Katherine E."],["dc.contributor.author","Yoon, Seungtai"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Corvin, Aiden"],["dc.contributor.author","Gary, Sydney"],["dc.contributor.author","Gershon, Elliot S."],["dc.contributor.author","Gill, Michael"],["dc.contributor.author","Karayiorgou, Maria"],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Krastoshevsky, Olga"],["dc.contributor.author","Krause, Verena"],["dc.contributor.author","Leibenluft, Ellen"],["dc.contributor.author","Levy, Deborah L."],["dc.contributor.author","Makarov, Vladimir"],["dc.contributor.author","Bhandari, Abhishek"],["dc.contributor.author","Malhotra, Anil K."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Potash, James B."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Sebat, Jonathan"],["dc.date.accessioned","2018-11-07T08:48:47Z"],["dc.date.available","2018-11-07T08:48:47Z"],["dc.date.issued","2011"],["dc.description.abstract","While it is known that rare copy-number variants (CNVs) contribute to risk for some neuropsychiatric disorders, the role of CNVs in bipolar disorder is unclear. Here, we reasoned that a contribution of CNVs to mood disorders might be most evident for de novo mutations. We performed a genome-wide analysis of de novo CNVs in a cohort of 788 trios. Diagnoses of offspring included bipolar disorder (n = 185), schizophrenia (n = 177), and healthy controls (n = 426). Frequencies of de novo CNVs were significantly higher in bipolar disorder as compared with controls (OR = 4.8 [1.4,16.0], p = 0.009). De novo CNVs were particularly enriched among cases with an age at onset younger than 18 (OR = 6.3 [1.7,22.6], p = 0.006). We also confirmed a significant enrichment of de novo CNVs in schizophrenia (OR = 5.0 [1.5,16.8], p = 0.007). Our results suggest that rare spontaneous mutations are an important contributor to risk for bipolar disorder and other major neuropsychiatric diseases."],["dc.identifier.doi","10.1016/j.neuron.2011.11.007"],["dc.identifier.isi","000298771000010"],["dc.identifier.pmid","22196331"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21306"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0896-6273"],["dc.title","High Frequencies of De Novo CNVs in Bipolar Disorder and Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1425"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics Part B Neuropsychiatric Genetics"],["dc.bibliographiccitation.lastpage","1433"],["dc.bibliographiccitation.volume","153B"],["dc.contributor.author","Mathieu, Flavie"],["dc.contributor.author","Dizier, Marie-Helene"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Albus, Margot"],["dc.contributor.author","McKeon, Patrick"],["dc.contributor.author","Roche, Siobhan"],["dc.contributor.author","Blackwood, Douglas"],["dc.contributor.author","Muir, Walter J."],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Malafosse, Alain"],["dc.contributor.author","Preisig, Martin"],["dc.contributor.author","Ferrero, Francois"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Ohlraun, Stephanie"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Abou Jamra, Rami"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Zelenica, Diana"],["dc.contributor.author","Charon, Celine"],["dc.contributor.author","Marusic, Andrej"],["dc.contributor.author","Dernovsek, Mojca C."],["dc.contributor.author","Gurling, Hugh"],["dc.contributor.author","Noethen, Markus"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Leboyer, Marion"],["dc.contributor.author","Bellivier, Frank"],["dc.date.accessioned","2018-11-07T08:35:56Z"],["dc.date.available","2018-11-07T08:35:56Z"],["dc.date.issued","2010"],["dc.description.abstract","Bipolar disorder has a genetic component, but the mode of inheritance remains unclear. A previous genome scan conducted in 70 European families led to detect eight regions linked to bipolar disease. Here, we present an investigation of whether the phenotypic heterogeneity of the disorder corresponds to genetic heterogeneity in these regions using additional markers and an extended sample of families. The MLS statistic was used for linkage analyses. The predivided sample test and the maximum likelihood binomial methods were used to test genetic homogeneity between early-onset bipolar type I (cut-off of 22 years) and other types of the disorder (later onset of bipolar type I and early-onset bipolar type II), using a total of 138 independent bipolar-affected sib-pairs. Analysis of the extended sample of families supports linkage in four regions (2q14, 3p14, 16p23, and 20p12) of the eight regions of linkage suggested by our previous genome scan. Heterogeneity testing revealed genetic heterogeneity between early and late-onset bipolar type I in the 2q14 region (P=0.0001). Only the early form of the bipolar disorder but not the late form appeared to be linked to this region. This region may therefore include a genetic factor either specifically involved in the early-onset bipolar type I or only influencing the age at onset (AAO). Our findings illustrate that stratification according to AAO may be valuable for the identification of genetic vulnerability polymorphisms. (C) 2010 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/ajmg.b.31121"],["dc.identifier.isi","000284623200006"],["dc.identifier.pmid","20886542"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18198"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1552-4841"],["dc.title","European Collaborative Study of Early-Onset Bipolar Disorder: Evidence for Genetic Heterogeneity on 2q14 According to Age at Onset"],["dc.type","journal_article"],["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.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.firstpage","35"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","42"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Havik, Bjarte"],["dc.contributor.author","Le Hellard, Stephanie"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Lybaek, Helle"],["dc.contributor.author","Djurovic, Srdjan"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Agartz, Ingrid"],["dc.contributor.author","Melle, Ingrid"],["dc.contributor.author","Hansen, Thomas C."],["dc.contributor.author","Bramham, Clive R."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Stevens, Beth"],["dc.contributor.author","Werge, Thomas"],["dc.contributor.author","Andreassen, Ole A."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Steen, Vidar M."],["dc.date.accessioned","2018-11-07T08:54:52Z"],["dc.date.available","2018-11-07T08:54:52Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: Patients with schizophrenia often suffer from cognitive dysfunction, including impaired learning and memory. We recently demonstrated that long-term potentiation in rat hippocampus, a mechanistic model of learning and memory, is linked to gene expression changes in immunity-related processes involved in complement activity and antigen presentation. We therefore aimed to examine whether key regulators of these processes are genetic susceptibility factors in schizophrenia. Methods: Analysis of genetic association was based on data mining of genotypes from a German genome-wide association study and a multiplex GoldenGate tag single nucleotide polymorphism (SNP)-based assay of Norwegian and Danish case-control samples (Scandinavian Collaboration on Psychiatric Etiology), including 1133 patients with schizophrenia and 2444 healthy control subjects. Results: Allelic associations were found across all three samples for eight common SNPs in the complement control-related gene CSMD2 (CUB and Sushi Multiple Domains 2) on chromosome 1p35.1-34.3, of which rs911213 reached a statistical significance comparable to that of a genome wide threshold (p value = 4.0 x 10(-8); odd ratio = .73, 95% confidence interval = .65-.82). The second most significant gene was CSMD1 on chromosome 8p23.2, a homologue to CSMD2. In addition, we observed replicated associations in the complement surface receptor CD46 as well as the major histocompatibility complex genes HLA-DMB and HLA-DOA. Conclusions: These data demonstrate a significant role of complement control-related genes in the etiology of schizophrenia and support disease mechanisms that involve the activity of immunity-related pathways in the brain."],["dc.identifier.doi","10.1016/j.biopsych.2011.01.030"],["dc.identifier.isi","000291559300009"],["dc.identifier.pmid","21439553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22773"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0006-3223"],["dc.title","The Complement Control-Related Genes CSMD1 and CSMD2 Associate to Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1294"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Schizophrenia Bulletin"],["dc.bibliographiccitation.lastpage","1308"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Luo, Xiong-Jian"],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Li, Ming"],["dc.contributor.author","Huang, Liang"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Borglum, Anders D."],["dc.contributor.author","Als, Thomas D."],["dc.contributor.author","van den Oord, Edwin J."],["dc.contributor.author","Aberg, Karolina A."],["dc.contributor.author","Mors, Ole"],["dc.contributor.author","Mortensen, Preben Bo"],["dc.contributor.author","Luo, Zhenwu"],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Su, Bing"],["dc.contributor.author","Zhao, Z."],["dc.contributor.author","Gan, Lin"],["dc.contributor.author","Yao, Yong-Gang"],["dc.date.accessioned","2018-11-07T09:49:28Z"],["dc.date.available","2018-11-07T09:49:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Genome-wide association studies have identified multiple risk variants and loci that show robust association with schizophrenia. Nevertheless, it remains unclear how these variants confer risk to schizophrenia. In addition, the driving force that maintains the schizophrenia risk variants in human gene pool is poorly understood. To investigate whether expression-associated genetic variants contribute to schizophrenia susceptibility, we systematically integrated brain expression quantitative trait loci and genome-wide association data of schizophrenia using Sherlock, a Bayesian statistical framework. Our analyses identified ZNF323 as a schizophrenia risk gene (P = 2.22x10(-6)). Subsequent analyses confirmed the association of the ZNF323 and its expression-associated single nucleotide polymorphism rs1150711 in independent samples (gene-expression: P = 1.40x10(-6); single-marker meta-analysis in the combined discovery and replication sample comprising 44123 individuals: (P = 6.85x10(-10)). We found that the ZNF323 was significantly downregulated in hippocampus and frontal cortex of schizophrenia patients (P = .0038 and P = .0233, respectively). Evidence for pleiotropic effects was detected (association of rs1150711 with lung function and gene expression of ZNF323 in lung: P = 6.62x10(-5) and P = 9.00x10(-5), respectively) with the risk allele (T allele) for schizophrenia acting as protective allele for lung function. Subsequent population genetics analyses suggest that the risk allele (T) of rs1150711 might have undergone recent positive selection in human population. Our findings suggest that the ZNF323 is a schizophrenia susceptibility gene whose expression may influence schizophrenia risk. Our study also illustrates a possible mechanism for maintaining schizophrenia risk variants in the human gene pool."],["dc.identifier.doi","10.1093/schbul/sbv017"],["dc.identifier.isi","000364774900015"],["dc.identifier.pmid","25759474"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35515"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1745-1701"],["dc.relation.issn","0586-7614"],["dc.title","Systematic Integration of Brain eQTL and GWAS Identifies ZNF323 as a Novel Schizophrenia Risk Gene and Suggests Recent Positive Selection Based on Compensatory Advantage on Pulmonary Function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Akula, Nirmala"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Steele, J. O."],["dc.contributor.author","Nalls, Michael A."],["dc.contributor.author","Singleton, Andrew B."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Noethen, Markus M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Mcmahon, Francis J."],["dc.date.accessioned","2018-11-07T09:42:18Z"],["dc.date.available","2018-11-07T09:42:18Z"],["dc.date.issued","2014"],["dc.description.abstract","Objectives. Genome-wide association studies (GWAS) in complex phenotypes, including psychiatric disorders, have yielded many replicated findings, yet individual markers account for only a small fraction of the inherited differences in risk. We tested the performance of polygenic models in discriminating between cases and healthy controls and among cases with distinct psychiatric diagnoses. Methods. GWAS results in bipolar disorder (BD), major depressive disorder (MDD), schizophrenia (SZ), and Parkinson's disease (PD) were used to assign weights to individual alleles, based on odds ratios. These weights were used to calculate allele scores for individual cases and controls in independent samples, summing across many single nucleotide polymorphisms (SNPs). How well allele scores discriminated between cases and controls and between cases with different disorders was tested by logistic regression. Results. Large sets of SNPs were needed to achieve even modest discrimination between cases and controls. The most informative SNPs were overlapping in BD, SZ, and MDD, with correlated effect sizes. Little or no overlap was seen between allele scores for psychiatric disorders and those for PD. Conclusions. BD, SZ, and MDD all share a similar polygenic component, but the polygenic models tested lack discriminative accuracy and are unlikely to be useful for clinical diagnosis."],["dc.identifier.doi","10.3109/15622975.2012.662282"],["dc.identifier.isi","000332798400004"],["dc.identifier.pmid","22404658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33926"],["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","Molecular genetic overlap in bipolar disorder, schizophrenia, and major depressive disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","433"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","444"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Willour, V. L."],["dc.contributor.author","Seifuddin, Fayaz"],["dc.contributor.author","Mahon, P. B."],["dc.contributor.author","Jancic, D."],["dc.contributor.author","Pirooznia, Mehdi"],["dc.contributor.author","Steele, Jo"],["dc.contributor.author","Schweizer, Barbara"],["dc.contributor.author","Goes, Fernando S."],["dc.contributor.author","Mondimore, F. M."],["dc.contributor.author","MacKinnon, D. F."],["dc.contributor.author","Perlis, Roy H."],["dc.contributor.author","Lee, Phil Hyoun"],["dc.contributor.author","Huang, J."],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Shilling, Paul D."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Noethen, M."],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Gurling, Hugh"],["dc.contributor.author","Purcell, Shaun M."],["dc.contributor.author","Smoller, Jordan W."],["dc.contributor.author","Craddock, N."],["dc.contributor.author","DePaulo, J. Raymond, Jr."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Zandi, Peter P."],["dc.contributor.author","Potash, James B."],["dc.date.accessioned","2018-11-07T09:11:54Z"],["dc.date.available","2018-11-07T09:11:54Z"],["dc.date.issued","2012"],["dc.description.abstract","The heritable component to attempted and completed suicide is partly related to psychiatric disorders and also partly independent of them. Although attempted suicide linkage regions have been identified on 2p11-12 and 6q25-26, there are likely many more such loci, the discovery of which will require a much higher resolution approach, such as the genome-wide association study (GWAS). With this in mind, we conducted an attempted suicide GWAS that compared the single-nucleotide polymorphism (SNP) genotypes of 1201 bipolar (BP) subjects with a history of suicide attempts to the genotypes of 1497 BP subjects without a history of suicide attempts. In all, 2507 SNPs with evidence for association at P < 0.001 were identified. These associated SNPs were subsequently tested for association in a large and independent BP sample set. None of these SNPs were significantly associated in the replication sample after correcting for multiple testing, but the combined analysis of the two sample sets produced an association signal on 2p25 (rs300774) at the threshold of genome-wide significance (P = 5.07 x 10(-8)). The associated SNPs on 2p25 fall in a large linkage disequilibrium block containing the ACP1 (acid phosphatase 1) gene, a gene whose expression is significantly elevated in BP subjects who have completed suicide. Furthermore, the ACP1 protein is a tyrosine phosphatase that influences Wnt signaling, a pathway regulated by lithium, making ACP1 a functional candidate for involvement in the phenotype. Larger GWAS sample sets will be required to confirm the signal on 2p25 and to identify additional genetic risk factors increasing susceptibility for attempted suicide. Molecular Psychiatry (2012) 17, 433-444; doi: 10.1038/mp.2011.4; published online 22 March 2011"],["dc.identifier.doi","10.1038/mp.2011.4"],["dc.identifier.isi","000302173900010"],["dc.identifier.pmid","21423239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26827"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","A genome-wide association study of attempted suicide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]