Kästner, Anne

[["dc.bibliographiccitation.firstpage","528"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","539"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hagemeyer, Nora"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Hofer, Sabine"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Heckers, Stephan H."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-08-25T10:14:17Z"],["dc.date.available","2017-08-25T10:14:17Z"],["dc.date.issued","2012"],["dc.description.abstract","Severe mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on mRNA and protein level in brains of schizophrenic, bipolar or major depressive patients. This suggests that CNP reduction might be critical for a more general disease process and not restricted to a single diagnostic category. We show here that reduced expression of CNP is the primary cause of a distinct behavioural phenotype, seen only upon aging as an additional 'pro-inflammatory hit'. This phenotype is strikingly similar in Cnp heterozygous mice and patients with mental disease carrying the AA genotype at CNP SNP rs2070106. The characteristic features in both species with their partial CNP 'loss-of-function' genotype are best described as 'catatonia-depression' syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, diffusion tensor imaging points to axonal loss in the frontal corpus callosum. To conclude, subtle white matter abnormalities inducing neurodegenerative changes can cause/amplify psychiatric diseases."],["dc.identifier.doi","10.1002/emmm.201200230"],["dc.identifier.gro","3150560"],["dc.identifier.pmid","22473874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7334"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A myelin gene causative of a catatonia-depression syndrome upon aging"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e254"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Klugmann, M."],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Monasterio-Schrader, P. D."],["dc.contributor.author","Strenzke, N."],["dc.contributor.author","Flügge, G."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Pawlak, R."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2013"],["dc.description.abstract","Claustrophobia, the well-known fear of being trapped in narrow/closed spaces, is often considered a conditioned response to traumatic experience. Surprisingly, we found that mutations affecting a single gene, encoding a stress-regulated neuronal protein, can cause claustrophobia. Gpm6a-deficient mice develop normally and lack obvious behavioral abnormalities. However, when mildly stressed by single-housing, these mice develop a striking claustrophobia-like phenotype, which is not inducible in wild-type controls, even by severe stress. The human GPM6A gene is located on chromosome 4q32-q34, a region linked to panic disorder. Sequence analysis of 115 claustrophobic and non-claustrophobic subjects identified nine variants in the noncoding region of the gene that are more frequent in affected individuals (P=0.028). One variant in the 3'untranslated region was linked to claustrophobia in two small pedigrees. This mutant mRNA is functional but cannot be silenced by neuronal miR124 derived itself from a stress-regulated transcript. We suggest that loosing dynamic regulation of neuronal GPM6A expression poses a genetic risk for claustrophobia."],["dc.format.extent","12"],["dc.identifier.doi","10.1038/tp.2013.28"],["dc.identifier.gro","3150562"],["dc.identifier.pmid","23632458"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7336"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.subject","chromosome 4; GPM6A; human pedigree; miR124; mouse mutant; panic disorder"],["dc.title","A single gene defect causing claustrophobia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","91"],["dc.bibliographiccitation.journal","BMC Psychiatry"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ackermann, Verena"],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Treitz, Annika"],["dc.contributor.author","Flögel, Marlene"],["dc.contributor.author","Adler, Lothar"],["dc.contributor.author","Aldenhoff, Josef B."],["dc.contributor.author","Becker-Emner, Marianne"],["dc.contributor.author","Becker, Thomas"],["dc.contributor.author","Czernik, Adelheid"],["dc.contributor.author","Dose, Matthias"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Freese, Roland"],["dc.contributor.author","Guenther, Rolf"],["dc.contributor.author","Herpertz, Sabine"],["dc.contributor.author","Hesse, Dirk"],["dc.contributor.author","Kruse, Gunther"],["dc.contributor.author","Kunze, Heinrich"],["dc.contributor.author","Franz, Michael"],["dc.contributor.author","Lohrer, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Mielke, Andreas"],["dc.contributor.author","Müller-Isberner, Rüdiger"],["dc.contributor.author","Oestereich, Cornelia"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Pollmächer, Thomas"],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Schwarz, Hans-Joachim"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Schizophrenia is the collective term for an exclusively clinically diagnosed, heterogeneous group of mental disorders with still obscure biological roots. Based on the assumption that valuable information about relevant genetic and environmental disease mechanisms can be obtained by association studies on patient cohorts of ≥ 1000 patients, if performed on detailed clinical datasets and quantifiable biological readouts, we generated a new schizophrenia data base, the GRAS (Göttingen Research Association for Schizophrenia) data collection. GRAS is the necessary ground to study genetic causes of the schizophrenic phenotype in a 'phenotype-based genetic association study' (PGAS). This approach is different from and complementary to the genome-wide association studies (GWAS) on schizophrenia. Methods: For this purpose, 1085 patients were recruited between 2005 and 2010 by an invariable team of traveling investigators in a cross-sectional field study that comprised 23 German psychiatric hospitals. Additionally, chart records and discharge letters of all patients were collected. Results: The corresponding dataset extracted and presented in form of an overview here, comprises biographic information, disease history, medication including side effects, and results of comprehensive cross-sectional psychopathological, neuropsychological, and neurological examinations. With >3000 data points per schizophrenic subject, this data base of living patients, who are also accessible for follow-up studies, provides a wide-ranging and standardized phenotype characterization of as yet unprecedented detail. Conclusions: The GRAS data base will serve as prerequisite for PGAS, a novel approach to better understanding 'the schizophrenias' through exploring the contribution of genetic variation to the schizophrenic phenotypes."],["dc.format.extent","20"],["dc.identifier.doi","10.1186/1471-244X-10-91"],["dc.identifier.gro","3150558"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5803"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7333"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The cross-sectional GRAS sample: a comprehensive phenotypical data collection of schizophrenic patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1029"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","1040"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Schwitulla, Judith"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Hannke, Kathrin"],["dc.contributor.author","Ramin, Anna"],["dc.contributor.author","Heinrich, Ralf"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2012"],["dc.description.abstract","Erythropoietin (EPO) improves cognitive performance in clinical studies and rodent experiments. We hypothesized that an intrinsicrole of EPO for cognition exists, with particular relevance in situations of cognitive decline, which is reflected by associations ofEPO and EPO receptor (EPOR) genotypes with cognitive functions. To prove this hypothesis, schizophrenic patients (N > 1000) weregenotyped for 5′ upstream–located gene variants, EPO SNP rs1617640 (T/G) and EPOR STR(GA)n. Associations of these variants wereobtained for cognitive processing speed, fine motor skills and short-term memory readouts, with one particular combination ofgenotypes superior to all others (p < 0.0001). In an independent healthy control sample (N > 800), these associations were confirmed.A matching preclinical study with mice demonstrated cognitive processing speed and memory enhanced upon transgenicexpression of constitutively active EPOR in pyramidal neurons of cortex and hippocampus. We thus predicted that thehuman genotypes associated with better cognition would reflect gain-of-function effects. Indeed, reporter gene assays and quantitativetranscriptional analysis of peripheral blood mononuclear cells showed genotype-dependent EPO/EPOR expression differences.Together, these findings reveal a role of endogenous EPO/EPOR for cognition, at least in schizophrenic patients."],["dc.identifier.doi","10.2119/molmed.2012.00190"],["dc.identifier.gro","3150561"],["dc.identifier.pmid","22669473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7335"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Common variants of the genes encoding erythropoietin and its receptor modulate cognitive performance in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e45"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malzahn, Dörte"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Stefansson, Hreinn"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:32Z"],["dc.date.available","2017-09-07T11:46:32Z"],["dc.date.issued","2011"],["dc.description.abstract","Genotype–phenotype correlations of common monogenic diseases revealed that the degree of deviation of mutant genes from wild-type structure and function often predicts disease onset and severity. In complex disorders such as schizophrenia, the overall genetic risk is still often >50% but genotype–phenotype relationships are unclear. Recent genome-wide association studies (GWAS) replicated a risk for several single-nucleotide polymorphisms (SNPs) regarding the endpoint diagnosis of schizophrenia. The biological relevance of these SNPs, however, for phenotypes or severity of schizophrenia has remained obscure. We hypothesized that the GWAS ‘top-10’ should as single markers, but even more so upon their accumulation, display associations with lead features of schizophrenia, namely positive and negative symptoms, cognitive deficits and neurological signs (including catatonia), and/or with age of onset of the disease prodrome as developmental readout and predictor of disease severity. For testing this hypothesis, we took an approach complementary to GWAS, and performed a phenotype-based genetic association study (PGAS). We utilized the to our knowledge worldwide largest phenotypical database of schizophrenic patients (n>1000), the GRAS (Göttingen Research Association for Schizophrenia) Data Collection. We found that the ‘top-10’ GWAS-identified risk SNPs neither as single markers nor when explored in the sense of a cumulative genetic risk, have any predictive value for disease onset or severity in the schizophrenic patients, as demonstrated across all core symptoms. We conclude that GWAS does not extract disease genes of general significance in schizophrenia, but may yield, on a hypothesis-free basis, candidate genes relevant for defining disease subgroups."],["dc.format.extent","6"],["dc.identifier.doi","10.1038/tp.2011.43"],["dc.identifier.gro","3150533"],["dc.identifier.pmid","22833191"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11388"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7305"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.subject","Cambridge neurological inventory; cognition; GWAS; PGAS; positive and negative syndrome scale; prodrome"],["dc.title","Dissociation of accumulated genetic risk and disease severity in patients with schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","218"],["dc.bibliographiccitation.journal","BMC Psychiatry"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Malzahn, Dörte"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Hilmes, Constanze"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:23Z"],["dc.date.available","2017-09-07T11:46:23Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Olfactory function tests are sensitive tools for assessing sensory-cognitive processing in schizophrenia. However, associations of central olfactory measures with clinical outcome parameters have not been simultaneously studied in large samples of schizophrenia patients. Methods: In the framework of the comprehensive phenotyping of the GRAS (Göttingen Research Association for Schizophrenia) cohort, we modified and extended existing odor naming (active memory retrieval) and interpretation (attribute assignment) tasks to evaluate them in 881 schizophrenia patients and 102 healthy controls matched for age, gender and smoking behavior. Associations with emotional processing, neuropsychological test performance and disease outcome were studied. Results: Schizophrenia patients underperformed controls in both olfactory tasks. Odor naming deficits were primarily associated with compromised cognition, interpretation deficits with positive symptom severity and general alertness. Contrasting schizophrenia extreme performers of odor interpretation (best versus worst percentile; N=88 each) and healthy individuals (N=102) underscores the obvious relationship between impaired odor interpretation and psychopathology, cognitive dysfunctioning, and emotional processing (all p<0.004). Conclusions: The strong association of performance in higher olfactory measures, odor naming and interpretation, with lead symptoms of schizophrenia and determinants of disease severity highlights their clinical and scientific significance. Based on the results obtained here in an exploratory fashion in a large patient sample, the development of an easy-to-use clinical test with improved psychometric properties may be encouraged."],["dc.format.extent","12"],["dc.identifier.doi","10.1186/1471-244X-13-218"],["dc.identifier.gro","3150490"],["dc.identifier.pmid","24229413"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9337"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7260"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Odor naming and interpretation performance in 881 schizophrenia subjects: association with clinical parameters"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","662"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","684"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Bodda, Chiranjeevi"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Castillo Venzor, Aracely"],["dc.contributor.author","Konte, Bettina"],["dc.contributor.author","Erbaba, Begun"],["dc.contributor.author","Hartmann, Annette M."],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Mannan, Ashraf U."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2014"],["dc.description.abstract","The X-chromosomal MECP2/Mecp2 gene encodes methyl-CpG-binding protein 2, a transcriptional activator and repressor regulating many other genes. We discovered in male FVB/N mice that mild (~50%) transgenic overexpression of Mecp2 enhances aggression. Surprisingly, when the same transgene was expressed in C57BL/6N mice, transgenics showed reduced aggression and social interaction. This suggests that Mecp2 modulates aggressive social behavior. To test this hypothesis in humans, we performed a phenotype-based genetic association study (PGAS) in >1000 schizophrenic individuals. We found MECP2 SNPs rs2239464 (G/A) and rs2734647 (C/T; 3'UTR) associated with aggression, with the G and C carriers, respectively, being more aggressive. This finding was replicated in an independent schizophrenia cohort. Allele-specific MECP2 mRNA expression differs in peripheral blood mononuclear cells by ~50% (rs2734647: C > T). Notably, the brain-expressed, species-conserved miR-511 binds to MECP2 3'UTR only in T carriers, thereby suppressing gene expression. To conclude, subtle MECP2/Mecp2 expression alterations impact aggression. While the mouse data provides evidence of an interaction between genetic background and mild Mecp2 overexpression, the human data convey means by which genetic variation affects MECP2 expression and behavior."],["dc.identifier.doi","10.1002/emmm.201303744"],["dc.identifier.gro","3150551"],["dc.identifier.pmid","24648499"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7325"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Mild expression differences of MECP2 influencing aggressive social behavior"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]