Kästner, Anne

[["dc.bibliographiccitation.artnumber","181"],["dc.bibliographiccitation.journal","Frontiers in Behavioral Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Lu, Derek"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Ju, Anes"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Chowdhury, Kamal"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2014"],["dc.description.abstract","Autism-spectrum disorders (ASD) are heterogeneous, highly heritable neurodevelopmental conditions affecting around 0.5% of the population across cultures, with a male/female ratio of approximately 4:1. Phenotypically, ASD are characterized by social interaction and communication deficits, restricted interests, repetitive behaviors, and reduced cognitive flexibility. Identified causes converge at the level of the synapse, ranging from mutation of synaptic genes to quantitative alterations in synaptic protein expression, e.g., through compromised transcriptional or translational control. We wondered whether reduced turnover and degradation of synapses, due to deregulated autophagy, would lead to similar phenotypical consequences. Ambra1, strongly expressed in cortex, hippocampus, and striatum, is a positive regulator of Beclin1, a principal player in autophagosome formation. While homozygosity of the Ambra1 null mutation causes embryonic lethality, heterozygous mice with reduced Ambra1 expression are viable, reproduce normally, and lack any immediately obvious phenotype. Surprisingly, comprehensive behavioral characterization of these mice revealed an autism-like phenotype in Ambra1 (+/-) females only, including compromised communication and social interactions, a tendency of enhanced stereotypies/repetitive behaviors, and impaired cognitive flexibility. Reduced ultrasound communication was found in adults as well as pups, which achieved otherwise normal neurodevelopmental milestones. These features were all absent in male Ambra1 (+/-) mice. As a first hint explaining this gender difference, we found a much stronger reduction of Ambra1 protein in the cortex of Ambra1 (+/-) females compared to males. To conclude, Ambra1 deficiency can induce an autism-like phenotype. The restriction to the female gender of autism-generation by a defined genetic trait is unique thus far and warrants further investigation."],["dc.format.extent","19"],["dc.identifier.doi","10.3389/fnbeh.2014.00181"],["dc.identifier.gro","3150538"],["dc.identifier.pmid","24904333"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11695"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7311"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject","Ambra1; autism composite score; autophagy; cognitive rigidity; heterozygous null mutant mice; repetitive behavior; social interaction; ultrasound communication"],["dc.title","Heterozygous Ambra1 deficiency in mice: a genetic trait with autism-like behavior restricted to the female gender"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","41"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","49"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Krueger, Dilja"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Ritter, Caroline"],["dc.contributor.author","Jatho, Jasmin"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Bourgeron, Thomas"],["dc.contributor.author","Fischer, Julia"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:47:38Z"],["dc.date.available","2017-09-07T11:47:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Autism is the short name of a complex and heterogeneous group of disorders (autism spectrum disorders, ASD) with several lead symptoms required for classification, including compromised social interaction, reduced verbal communication and stereotyped repetitive behaviors/restricted interests. The etiology of ASD is still unknown in most cases but monogenic heritable forms exist that have provided insights into ASD pathogenesis and have led to the notion of autism as a 'synapse disorder'. Among the most frequent monogenic causes of autism are loss-of-function mutations of the NLGN4X gene which encodes the synaptic cell adhesion protein neuroligin-4X (NLGN4X). We previously described autism-like behaviors in male Nlgn4 null mutant mice, including reduced social interaction and ultrasonic communication. Here, we extend the phenotypical characterization of Nlgn4 null mutant mice to both genders and add a series of additional autism-relevant behavioral readouts. We now report similar social interaction and ultrasonic communication deficits in females as in males. Furthermore, aggression, nest-building parameters, as well as self-grooming and circling as indicators of repetitive behaviors/stereotypies were explored in both genders. The construction of a gender-specific autism severity composite score for Nlgn4 mutant mice markedly diminishes population/sample heterogeneity typically obtained for single tests, resulting in p values of <0.00001 and a genotype predictability of 100% for male and of >83% for female mice. Taken together, these data underscore the similarity of phenotypical consequences of Nlgn4/NLGN4X loss-of-function in mouse and man, and emphasize the high relevance of Nlgn4 null mutant mice as an ASD model with both construct and face validity."],["dc.identifier.doi","10.1016/j.bbr.2012.11.016"],["dc.identifier.gro","3142307"],["dc.identifier.isi","000322927700006"],["dc.identifier.pmid","23183221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6831"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0166-4328"],["dc.subject","Social interaction; Nest building; Grooming; Repetitive behaviors; Stereotypies; Ultra-sound vocalization; Gender differences; ASD"],["dc.title","Development of an autism severity score for mice using Nlgn4 null mutants as a construct-valid model of heritable monogenic autism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","95"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Der Anaesthesist"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Erlenwein, J."],["dc.contributor.author","Pfingsten, M."],["dc.contributor.author","Hüppe, M."],["dc.contributor.author","Seeger, D."],["dc.contributor.author","Kästner, A."],["dc.contributor.author","Graner, R."],["dc.contributor.author","Petzke, F."],["dc.date.accessioned","2020-12-10T14:08:07Z"],["dc.date.available","2020-12-10T14:08:07Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00101-019-00708-2"],["dc.identifier.eissn","1432-055X"],["dc.identifier.issn","0003-2417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70378"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.haserratum","/handle/2/70384"],["dc.title","Management von Patienten mit chronischen Schmerzen in der Akut- und perioperativen Medizin"],["dc.title.alternative","Management of patients with chronic pain in acute and perioperative medicine. An interdisciplinary challenge"],["dc.title.subtitle","Eine interdisziplinäre Herausforderung"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","144"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","151"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Castillo-Gomez, Esther"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Hettling, Bilke"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Ostehr, Kristin"],["dc.contributor.author","Uhr, Manfred"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Matzke, Mike"],["dc.contributor.author","Schmidt, Ulrike"],["dc.contributor.author","Pfander, Viktoria"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Schulz, Thomas F."],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Weber, Frank"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are highly seroprevalent in health and disease. Symptomatic relevance may arise upon compromised blood–brain barrier (BBB). However, it remained unknown whether circulating NMDAR1 AB appear in the cerebrospinal fluid (CSF). Of n = 271 subjects with CSF–serum pairs, 26 were NMDAR1 AB seropositive, but only 1 was CSF positive. Contrariwise, tetanus AB (non–brain-binding) were present in serum and CSF of all subjects, with CSF levels higher upon BBB dysfunction. Translational mouse experiments proved the hypothesis that the brain acts as an ‘immunoprecipitator’; simultaneous injection of NMDAR1 AB and the non–brain-binding green fluorescent protein AB resulted in high detectability of the former in brain and the latter in CSF."],["dc.identifier.doi","10.1002/ana.24545"],["dc.identifier.gro","3150536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7309"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0364-5134"],["dc.title","The brain as immunoprecipitator of serum autoantibodies against N-Methyl-D-aspartate receptor subunit NR1"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["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.firstpage","330"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Der Anaesthesist"],["dc.bibliographiccitation.lastpage","330"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Erlenwein, J."],["dc.contributor.author","Pfingsten, M."],["dc.contributor.author","Hüppe, M."],["dc.contributor.author","Seeger, D."],["dc.contributor.author","Kästner, A."],["dc.contributor.author","Graner, R."],["dc.contributor.author","Petzke, F."],["dc.date.accessioned","2020-12-10T14:08:08Z"],["dc.date.available","2020-12-10T14:08:08Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00101-020-00759-w"],["dc.identifier.eissn","1432-055X"],["dc.identifier.issn","0003-2417"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70384"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.iserratumof","/handle/2/70378"],["dc.title","Erratum zu: Management von Patienten mit chronischen Schmerzen in der Akut- und perioperativen Medizin"],["dc.title.alternative","Erratum to: Management of patients with chronic pain in acute and perioperativemedicine. An interdisciplinary challenge"],["dc.title.subtitle","Eine interdisziplinäre Herausforderung"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Minerva Anestesiologica"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Ng Kuet Leong, Virginie S."],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Petzke, Frank"],["dc.contributor.author","Przemeck, Michael"],["dc.contributor.author","Erlenwein, Joachim"],["dc.date.accessioned","2021-04-14T08:32:41Z"],["dc.date.available","2021-04-14T08:32:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.23736/S0375-9393.20.14084-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83983"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1827-1596"],["dc.relation.issn","0375-9393"],["dc.title","The influence of pain expectation on pain experience after orthopedic surgery: an observational cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1306"],["dc.bibliographiccitation.issue","11-12"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","1310"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Streeter, Jackson"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Wang, Kevin K."],["dc.contributor.author","Worthmann, Hans"],["dc.contributor.author","Hayes, Ronald L."],["dc.contributor.author","Ahsen, Nico von"],["dc.contributor.author","Kastrup, Andreas"],["dc.contributor.author","Jeromin, Andreas"],["dc.contributor.author","Herrmann, Manfred"],["dc.date.accessioned","2017-09-07T11:46:19Z"],["dc.date.available","2017-09-07T11:46:19Z"],["dc.date.issued","2011"],["dc.description.abstract","The German Multicenter EPO Stroke Trial, which investigated safety and efficacy of erythropoietin (EPO) treatment in ischemic stroke, was formally declared a negative study. Exploratory subgroup analysis, however, revealed that patients not receiving thrombolysis most likely benefited from EPO during clinical recovery, a result demonstrated in the findings of the Göttingen EPO Stroke Study. The present work investigated whether the positive signal on clinical outcome in this patient subgroup was mirrored by respective poststroke biomarker profiles. All patients of the German Multicenter EPO Stroke Trial nonqualifying for thrombolysis were included if they (a) were treated per protocol and (b) had at least two of the five follow-up blood samples for circulating damage markers drawn (n = 163). The glial markers S100B and glial fibrillary acid protein (GFAP) and the neuronal marker ubiquitin C-terminal hydrolase (UCH-L1) were measured by enzyme-linked immunosorbent assay in serum on d 1, 2, 3, 4 and 7 poststroke. All biomarkers increased poststroke. Overall, EPO-treated patients had significantly lower concentrations (area under the curve) over 7 d of observation, as reflected by the composite score of all three markers (Cronbach α = 0.811) and by UCH-L1. S100B and GFAP showed a similar tendency. To conclude, serum biomarker profiles, as an outcome measure of brain damage, corroborate an advantageous effect of EPO in ischemic stroke. In particular, reduction in the neuronal damage marker UCH-L1 may reflect neuroprotection by EPO."],["dc.identifier.doi","10.2119/molmed.2011.00259"],["dc.identifier.gro","3150486"],["dc.identifier.pmid","21912808"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7256"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Circulating damage marker profiles support a neuroprotective effect of erythropoietin in ischemic stroke patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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"]]