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","140"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Human Brain Mapping"],["dc.bibliographiccitation.lastpage","151"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Esslinger, Christine"],["dc.contributor.author","Schueler, Nadja"],["dc.contributor.author","Sauer, Carina"],["dc.contributor.author","Gass, Dagmar"],["dc.contributor.author","Mier, Daniela"],["dc.contributor.author","Braun, Urs"],["dc.contributor.author","Ochs, Elisabeth"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Kirsch, Peter"],["dc.contributor.author","Meyer-Lindenberg, Andreas"],["dc.date.accessioned","2018-11-07T09:47:17Z"],["dc.date.available","2018-11-07T09:47:17Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuronal plasticity is crucial for flexible interaction with a changing environment and its disruption is thought to contribute to psychiatric diseases like schizophrenia. High-frequency repetitive transcranial magnetic stimulation (rTMS) is a noninvasive tool to increase local excitability of neurons and induce short-time functional reorganization of cortical networks. While this has been shown for the motor system, little is known about the short-term plasticity of networks for executive cognition in humans. We examined 12 healthy control subjects in a crossover study with fMRI after real and sham 5 Hz rTMS to the right dorsolateral prefrontal cortex (DLPFC). During scanning, subjects performed an n-back working memory (WM) task and a flanker task engaging cognitive control. Reaction times during the n-back task were significantly shorter after rTMS than after sham stimulation. RTMS compared with sham stimulation caused no activation changes at the stimulation site (right DLPFC) itself, but significantly increased connectivity within the WM network during n-back and reduced activation in the anterior cingulate cortex during the flanker task. Reduced reaction times after real stimulation support an excitatory effect of high-frequency rTMS. Our findings identified plastic changes in prefrontally connected networks downstream of the stimulation site as the substrate of this behavioral effect. Using a multimodal fMRI-rTMS approach, we could demonstrate changes in cortical plasticity in humans during executive cognition. In further studies this approach could be used to study pharmacological, genetic and disease-related alterations. Hum Brain Mapp 35:140-151, 2014. (c) 2012 Wiley Periodicals, Inc."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [Sonderforschungsbereich SFB 636]"],["dc.identifier.doi","10.1002/hbm.22165"],["dc.identifier.isi","000327859900011"],["dc.identifier.pmid","22965696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35075"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0193"],["dc.relation.issn","1065-9471"],["dc.title","Induction and Quantification of Prefrontal Cortical Network Plasticity Using 5 Hz rTMS and fMRI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","65"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Kamer, Thomas"],["dc.contributor.author","Roy, Anand"],["dc.contributor.author","Vogeley, Kai"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Schild, Hans H."],["dc.contributor.author","Block, Wolfgang"],["dc.contributor.author","Traeber, Frank"],["dc.contributor.author","Tepest, Ralf"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T11:19:33Z"],["dc.date.available","2018-11-07T11:19:33Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: The anterior limb of the internal capsule (ALIC), connecting cortical and subcortical structures, is involved in functional important circuits. To detect volumetric changes in ALIC, including the influence of genetic factors, a magnetic resonance imaging (MRI) study of families affected with schizophrenia was performed. Methods: The study sample comprised 22 family members with schizophrenia (FM-SZ), 34 family members without schizophrenia (FM-NSZ), and 43 control subjects. In addition to manual tracing of ALIC, subjects underwent proton magnetic resonance spectroscopy in the left prefrontal cortex, psychopathological rating, and neuropsychological assessment of frontal lobe function. Results: Compared with controls, a significant reduction of right ALIC volume was seen in all family members (12%-16% reduction, p <.01) and a reduction of left ALIC volume in FM-NSZ (10% reduction, p =.028) was also observed. Both groups of family members showed a bilateral reduction in maximal cross sectional area of the ALIC. FM-SZ performed significantly worse on neurocognitive measures (Subject Ordered Pointing Task [SOPT] and Wisconsin Card Sorting Test), and performance correlated negatively with the ALIC volume (SOPT, r = -.6, p =.03). Conclusions: A reduced volume of ALIC in affected families supports the hypothesis of disturbed frontothalamic connectivity in schizophrenia and demonstrates functional relevance by an association with reduced neurocognitive performance."],["dc.identifier.doi","10.1016/j.biopsych.2007.02.026"],["dc.identifier.isi","000251864000011"],["dc.identifier.pmid","17574215"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55310"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0006-3223"],["dc.title","Reduction of the internal capsule in families affected with schizophrenia"],["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.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","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"]]