Schulze, Thomas Gerd

[["dc.bibliographiccitation.artnumber","15351"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Rietschel, Liz"],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Zhu, Gu"],["dc.contributor.author","McAloney, Kerrie"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Couvy-Duchesne, Baptiste"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Binz, Tina M."],["dc.contributor.author","McGrath, John"],["dc.contributor.author","Hickie, Ian B."],["dc.contributor.author","Hansell, Narelle K."],["dc.contributor.author","Wright, Margaret J."],["dc.contributor.author","Gillespie, Nathan A."],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Wüst, Stefan"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Baumgartner, Markus R."],["dc.contributor.author","Walker, Brian R."],["dc.contributor.author","Crawford, Andrew A."],["dc.contributor.author","Colodro-Conde, Lucía"],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2019-07-09T11:44:40Z"],["dc.date.available","2019-07-09T11:44:40Z"],["dc.date.issued","2017-11-10"],["dc.description.abstract","Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables."],["dc.identifier.doi","10.1038/s41598-017-11852-3"],["dc.identifier.pmid","29127340"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14860"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59064"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Hair Cortisol in Twins: Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.lastpage","75"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Kalman, Janos L."],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Adli, Mazda"],["dc.contributor.author","Adorjan, Kristina"],["dc.contributor.author","Akula, Nirmala"],["dc.contributor.author","Alda, Martin"],["dc.contributor.author","Schulze, Thomas G."],["dc.date.accessioned","2019-07-09T11:50:29Z"],["dc.date.available","2019-07-09T11:50:29Z"],["dc.date.issued","2019"],["dc.description.abstract","OBJECTIVES: Bipolar disorder (BD) with early disease onset is associated with an unfavorable clinical outcome and constitutes a clinically and biologically homogenous subgroup within the heterogeneous BD spectrum. Previous studies have found an accumulation of early age at onset (AAO) in BD families and have therefore hypothesized that there is a larger genetic contribution to the early-onset cases than to late onset BD. To investigate the genetic background of this subphenotype, we evaluated whether an increased polygenic burden of BD- and schizophrenia (SCZ)-associated risk variants is associated with an earlier AAO in BD patients. METHODS: A total of 1995 BD type 1 patients from the Consortium of Lithium Genetics (ConLiGen), PsyCourse and Bonn-Mannheim samples were genotyped and their BD and SCZ polygenic risk scores (PRSs) were calculated using the summary statistics of the Psychiatric Genomics Consortium as a training data set. AAO was either separated into onset groups of clinical interest (childhood and adolescence [≤18 years] vs adulthood [>18 years]) or considered as a continuous measure. The associations between BD- and SCZ-PRSs and AAO were evaluated with regression models. RESULTS: BD- and SCZ-PRSs were not significantly associated with age at disease onset. Results remained the same when analyses were stratified by site of recruitment. CONCLUSIONS: The current study is the largest conducted so far to investigate the association between the cumulative BD and SCZ polygenic risk and AAO in BD patients. The reported negative results suggest that such a polygenic influence, if there is any, is not large, and highlight the importance of conducting further, larger scale studies to obtain more information on the genetic architecture of this clinically relevant phenotype."],["dc.identifier.doi","10.1111/bdi.12659"],["dc.identifier.pmid","29956436"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15948"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59781"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1399-5618"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Investigating polygenic burden in age at disease onset in bipolar disorder: Findings from an international multicentric study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","156"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology : The Journal of the European College of Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Friedrichs, Stefanie"],["dc.contributor.author","Alliey-Rodriguez, Ney"],["dc.contributor.author","Ament, Seth"],["dc.contributor.author","Badner, Judith A."],["dc.contributor.author","Berrettini, Wade H."],["dc.contributor.author","Bloss, Cinnamon S."],["dc.contributor.author","Byerley, William"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Comes, Ashley L."],["dc.contributor.author","Coryell, William"],["dc.contributor.author","Craig, David W."],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Edenberg, Howard J."],["dc.contributor.author","Foroud, Tatiana"],["dc.contributor.author","Forstner, Andreas J."],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Gershon, Elliot S."],["dc.contributor.author","Goes, Fernando S."],["dc.contributor.author","Greenwood, Tiffany A."],["dc.contributor.author","Guo, Yiran"],["dc.contributor.author","Hipolito, Maria"],["dc.contributor.author","Hood, Leroy"],["dc.contributor.author","Keating, Brendan J."],["dc.contributor.author","Koller, Daniel L."],["dc.contributor.author","Lawson, William B."],["dc.contributor.author","Liu, Chunyu"],["dc.contributor.author","Mahon, Pamela B."],["dc.contributor.author","McInnis, Melvin G."],["dc.contributor.author","McMahon, Francis J."],["dc.contributor.author","Meier, Sandra M."],["dc.contributor.author","Mühleisen, Thomas W."],["dc.contributor.author","Murray, Sarah S."],["dc.contributor.author","Nievergelt, Caroline M."],["dc.contributor.author","Nurnberger, John I."],["dc.contributor.author","Nwulia, Evaristus A."],["dc.contributor.author","Potash, James B."],["dc.contributor.author","Quarless, Danjuma"],["dc.contributor.author","Rice, John"],["dc.contributor.author","Roach, Jared C."],["dc.contributor.author","Scheftner, William A."],["dc.contributor.author","Schork, Nicholas J."],["dc.contributor.author","Shekhtman, Tatyana"],["dc.contributor.author","Shilling, Paul D."],["dc.contributor.author","Smith, Erin N."],["dc.contributor.author","Streit, Fabian"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Szelinger, Szabolcs"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Zandi, Peter P."],["dc.contributor.author","Zhang, Peng"],["dc.contributor.author","Zöllner, Sebastian"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Falkai, Peter G."],["dc.contributor.author","Kelsoe, John R."],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Malzahn, Dörthe"],["dc.date.accessioned","2019-07-09T11:50:26Z"],["dc.date.available","2019-07-09T11:50:26Z"],["dc.date.issued","2019-"],["dc.description.abstract","Genome-wide association studies of case-control status have advanced the understanding of the genetic basis of psychiatric disorders. Further progress may be gained by increasing sample size but also by new analysis strategies that advance the exploitation of existing data, especially for clinically important quantitative phenotypes. The functionally-informed efficient region-based test strategy (FIERS) introduced herein uses prior knowledge on biological function and dependence of genotypes within a powerful statistical framework with improved sensitivity and specificity for detecting consistent genetic effects across studies. As proof of concept, FIERS was used for the first genome-wide single nucleotide polymorphism (SNP)-based investigation on bipolar disorder (BD) that focuses on an important aspect of disease course, the functional outcome. FIERS identified a significantly associated locus on chromosome 15 (hg38: chr15:48965004 - 49464789 bp) with consistent effect strength between two independent studies (GAIN/TGen: European Americans, BOMA: Germans; n = 1592 BD patients in total). Protective and risk haplotypes were found on the most strongly associated SNPs. They contain a CTCF binding site (rs586758); CTCF sites are known to regulate sets of genes within a chromatin domain. The rs586758 - rs2086256 - rs1904317 haplotype is located in the promoter flanking region of the COPS2 gene, close to microRNA4716, and the EID1, SHC4, DTWD1 genes as plausible biological candidates. While implication with BD is novel, COPS2, EID1, and SHC4 are known to be relevant for neuronal differentiation and function and DTWD1 for psychopharmacological side effects. The test strategy FIERS that enabled this discovery is equally applicable for tag SNPs and sequence data."],["dc.identifier.doi","10.1016/j.euroneuro.2018.10.005"],["dc.identifier.pmid","30503783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59772"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1873-7862"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Efficient region-based test strategy uncovers genetic risk factors for functional outcome in bipolar disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]