Boretius, Susann

[["dc.bibliographiccitation.firstpage","592"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Genes, Brain and Behavior"],["dc.bibliographiccitation.lastpage","602"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Castaneda, S."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Bickeböller, H."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Brose, N."],["dc.contributor.author","Ehrenreich, Hanhelore"],["dc.date.accessioned","2017-09-07T11:45:21Z"],["dc.date.available","2017-09-07T11:45:21Z"],["dc.date.issued","2010"],["dc.description.abstract","Schizophrenia is a devastating disease that affects approximately 1% of the population across cultures. Its neurobiological underpinnings are still unknown. Accordingly, animal models of schizophrenia often lack construct validity. As concordance rate in monozygotic twins amounts to only 50%, environmental risk factors (e.g. neurotrauma, drug abuse, psychotrauma) likely act as necessary 'second hit' to trigger/drive the disease process in a genetically predisposed individual. Valid animal models would have to consider this genetic-environmental interaction. Based on this concept, we designed an experimental approach for modeling a schizophrenia-like phenotype in mice. As dysfunction in synaptic transmission plays a key role in schizophrenia, and complexin2 (CPLX2) gene expression is reduced in hippocampus of schizophrenic patients, we developed a mouse model with Cplx2 null mutation as genetic risk factor and a mild parietal neurotrauma, applied during puberty, as environmental 'second hit'. Several months after lesion, Cplx2 null mutants showed reduced pre-pulse inhibition, deficit of spatial learning and loss of inhibition after MK-801 challenge. These abnormalities were largely absent in lesioned wild-type mice and non-lesioned Cplx2 null mutants. Forced alternation in T-maze, object recognition, social interaction and elevated plus maze tests were unaltered in all groups. The previously reported mild motor phenotype of Cplx2 null mutants was accentuated upon lesion. MRI volumetrical analysis showed a decrease of hippocampal volume exclusively in lesioned Cplx2 null mutants. These findings provide suggestive evidence for the 'second hit' hypothesis of schizophrenia and may offer new tools for the development of advanced treatment strategies."],["dc.identifier.doi","10.1111/j.1601-183X.2010.00590.x"],["dc.identifier.gro","3142880"],["dc.identifier.isi","000281032700005"],["dc.identifier.pmid","20412316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/332"],["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","1601-1848"],["dc.title","Complexin2 null mutation requires a 'second hit' for induction of phenotypic changes relevant to schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8634"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","8647"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Garcia-Agudo, Laura Fernandez"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Sendler, Lea E."],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Steixner, Agnes A."],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Balmuth, Evan"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Schopf, Nadine"],["dc.contributor.author","Flier, Felicia J."],["dc.contributor.author","Ehrenreich, And Hannelore"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2022-10-06T13:35:25Z"],["dc.date.available","2022-10-06T13:35:25Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1096/fj.201900337R"],["dc.identifier.eissn","1530-6860"],["dc.identifier.issn","0892-6638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116091"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Genetically induced brain inflammation by\r\n Cnp\r\n deletion transiently benefits from microglia depletion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","1489"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1501"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Pan, Hong"],["dc.contributor.author","Oliveira, Bárbara"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Tapken, Daniel"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Seidel, Jan"],["dc.contributor.author","Wesolowski, Janina"],["dc.contributor.author","Wakhloo, Debia"],["dc.contributor.author","Klein-Schmidt, Christina"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Schwabe, Kerstin"],["dc.contributor.author","Trippe, Ralf"],["dc.contributor.author","Mätz-Rensing, Kerstin"],["dc.contributor.author","Berghoff, Stefan"],["dc.contributor.author","Al-Krinawe, Yazeed"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Mischke, Reinhard"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Krauss, Joachim K."],["dc.contributor.author","Hollmann, Michael"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T18:09:36Z"],["dc.date.available","2020-12-10T18:09:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41380-017-0011-3"],["dc.identifier.eissn","1476-5578"],["dc.identifier.issn","1359-4184"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15575"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73703"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-SA 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/4.0"],["dc.title","Uncoupling the widespread occurrence of anti-NMDAR1 autoantibodies from neuropsychiatric disease in a novel autoimmune model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","121"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wilke, Justus B. H."],["dc.contributor.author","Hindermann, Martin"],["dc.contributor.author","Moussavi, Amir"],["dc.contributor.author","Butt, Umer J."],["dc.contributor.author","Dadarwal, Rakshit"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Sarcheshmeh, Aref K."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Zihsler, Svenja"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Hardeland, Rüdiger"],["dc.contributor.author","Seidel, Jan"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2021-11-25T11:24:44Z"],["dc.date.accessioned","2022-08-18T12:41:08Z"],["dc.date.available","2021-11-25T11:24:44Z"],["dc.date.available","2022-08-18T12:41:08Z"],["dc.date.issued","2021-07-02"],["dc.date.updated","2022-07-29T12:18:38Z"],["dc.description.abstract","Abstract\r\n Up to one person in a population of 10,000 is diagnosed once in lifetime with an encephalitis, in 50–70% of unknown origin. Recognized causes amount to 20–50% viral infections. Approximately one third of affected subjects develops moderate and severe subsequent damage. Several neurotropic viruses can directly infect pyramidal neurons and induce neuronal death in cortex and hippocampus. The resulting encephalitic syndromes are frequently associated with cognitive deterioration and dementia, but involve numerous parallel and downstream cellular and molecular events that make the interpretation of direct consequences of sudden pyramidal neuronal loss difficult. This, however, would be pivotal for understanding how neuroinflammatory processes initiate the development of neurodegeneration, and thus for targeted prophylactic and therapeutic interventions. Here we utilized adult male NexCreERT2xRosa26-eGFP-DTA (= ‘DTA’) mice for the induction of a sterile encephalitis by diphtheria toxin-mediated ablation of cortical and hippocampal pyramidal neurons which also recruits immune cells into gray matter. We report multifaceted aftereffects of this defined process, including the expected pathology of classical hippocampal behaviors, evaluated in Morris water maze, but also of (pre)frontal circuit function, assessed by prepulse inhibition. Importantly, we modelled in encephalitis mice novel translationally relevant sequelae, namely altered social interaction/cognition, accompanied by compromised thermoreaction to social stimuli as convenient readout of parallel autonomic nervous system (dys)function. High resolution magnetic resonance imaging disclosed distinct abnormalities in brain dimensions, including cortical and hippocampal layering, as well as of cerebral blood flow and volume. Fluorescent tracer injection, immunohistochemistry and brain flow cytometry revealed persistent blood–brain-barrier perturbance and chronic brain inflammation. Surprisingly, blood flow cytometry showed no abnormalities in circulating major immune cell subsets and plasma high-mobility group box 1 (HMGB1) as proinflammatory marker remained unchanged. The present experimental work, analyzing multidimensional outcomes of direct pyramidal neuronal loss, will open new avenues for urgently needed encephalitis research."],["dc.identifier.citation","Acta Neuropathologica Communications. 2021 Jul 02;9(1):121"],["dc.identifier.doi","10.1186/s40478-021-01214-6"],["dc.identifier.pii","1214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112989"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","BioMed Central"],["dc.relation.eissn","2051-5960"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Diphtheria toxin"],["dc.subject","Hippocampal learning and memory"],["dc.subject","(pre)frontal network dysfunction"],["dc.subject","Social cognition"],["dc.subject","Thermography"],["dc.subject","Magnetic resonance imaging"],["dc.title","Inducing sterile pyramidal neuronal death in mice to model distinct aspects of gray matter encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]