Boretius, Susann

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Mitjans, M."],["dc.contributor.author","Begemann, M."],["dc.contributor.author","Ju, A."],["dc.contributor.author","Dere, E."],["dc.contributor.author","Wüstefeld, L."],["dc.contributor.author","Hofer, S."],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Balkenhol, J."],["dc.contributor.author","Oliveira, B."],["dc.contributor.author","van der Auwera, S."],["dc.contributor.author","Tammer, R."],["dc.contributor.author","Hammerschmidt, K."],["dc.contributor.author","Völzke, H."],["dc.contributor.author","Homuth, G."],["dc.contributor.author","Cecconi, F."],["dc.contributor.author","Chowdhury, K."],["dc.contributor.author","Grabe, H."],["dc.contributor.author","Frahm, J."],["dc.contributor.author","Boretius, S."],["dc.contributor.author","Dandekar, T."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-03-08T09:22:12Z"],["dc.date.available","2018-03-08T09:22:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Ambra1 is linked to autophagy and neurodevelopment. Heterozygous Ambra1 deficiency induces autism-like behavior in a sexually dimorphic manner. Extraordinarily, autistic features are seen in female mice only, combined with stronger Ambra1 protein reduction in brain compared to males. However, significance of AMBRA1 for autistic phenotypes in humans and, apart from behavior, for other autism-typical features, namely early brain enlargement or increased seizure propensity, has remained unexplored. Here we show in two independent human samples that a single normal AMBRA1 genotype, the intronic SNP rs3802890-AA, is associated with autistic features in women, who also display lower AMBRA1 mRNA expression in peripheral blood mononuclear cells relative to female GG carriers. Located within a non-coding RNA, likely relevant for mRNA and protein interaction, rs3802890 (A versus G allele) may affect its stability through modification of folding, as predicted by in silico analysis. Searching for further autism-relevant characteristics in Ambra1+/− mice, we observe reduced interest of female but not male mutants regarding pheromone signals of the respective other gender in the social intellicage set-up. Moreover, altered pentylentetrazol-induced seizure propensity, an in vivo readout of neuronal excitation–inhibition dysbalance, becomes obvious exclusively in female mutants. Magnetic resonance imaging reveals mild prepubertal brain enlargement in both genders, uncoupling enhanced brain dimensions from the primarily female expression of all other autistic phenotypes investigated here. These data support a role of AMBRA1/Ambra1 partial loss-of-function genotypes for female autistic traits. Moreover, they suggest Ambra1 heterozygous mice as a novel multifaceted and construct-valid genetic mouse model for female autism."],["dc.identifier.doi","10.1038/tp.2017.213"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12914"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.doi","10.1038/tp.2017.213"],["dc.relation.issn","2158-3188"],["dc.relation.issn","2158-3188"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Sexual dimorphism of AMBRA1-related autistic features in human and mouse"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","416"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Genes, Brain and Behavior"],["dc.bibliographiccitation.lastpage","425"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Radyushkin, K."],["dc.contributor.author","Hammerschmidt, K."],["dc.contributor.author","Boretius, S."],["dc.contributor.author","Varoqueaux, F."],["dc.contributor.author","El-Kordi, A."],["dc.contributor.author","Ronnenberg, A."],["dc.contributor.author","Winter, D."],["dc.contributor.author","Frahm, J."],["dc.contributor.author","Fischer, J."],["dc.contributor.author","Brose, N."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-08-25T10:14:23Z"],["dc.date.available","2017-08-25T10:14:23Z"],["dc.date.issued","2009"],["dc.description.abstract","Autism spectrum disorder (ASD) is a frequent neurodevelopmental disorder characterized by variable clinical severity. Core symptoms are qualitatively impaired communication and social behavior, highly restricted interests and repetitive behaviors. Although recent work on genetic mutations in ASD has shed light on the pathophysiology of the disease, classifying it essentially as a synaptopathy, no treatments are available to date. To develop and test novel ASD treatment approaches, validated and informative animal models are required. Of particular interest, in this context are loss-of-function mutations in the postsynaptic cell adhesion protein neuroligin-4 and point mutations in its homologue neuroligin-3 (NL-3) that were found to cause certain forms of monogenic heritable ASD in humans. Here, we show that NL-3-deficient mice display a behavioral phenotype reminiscent of the lead symptoms of ASD: reduced ultrasound vocalization and a lack of social novelty preference. The latter may be related to an olfactory deficiency observed in the NL-3 mutants. Interestingly, such olfactory phenotype is also present in a subgroup of human ASD patients. Tests for learning and memory showed no gross abnormalities in NL-3 mutants. Also, no alterations were found in time spent in social interaction, prepulse inhibition, seizure propensity and sucrose preference. As often seen in adult ASD patients, total brain volume of NL-3 mutant mice was slightly reduced as assessed by magnetic resonance imaging (MRI). Our findings show that the NL-3 knockout mouse represents a useful animal model for understanding pathophysiological events in monogenic heritable ASD and for developing novel treatment strategies in this devastating human disorder."],["dc.identifier.doi","10.1111/j.1601-183x.2009.00487.x"],["dc.identifier.gro","3150625"],["dc.identifier.pmid","19243448"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7403"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1601-1848"],["dc.title","Neuroligin-3-deficient mice: model of a monogenic heritable form of autism with an olfactory deficit"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","628"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","635"],["dc.contributor.author","Hagemeyer, Nora"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Von Streitberg, Axel"],["dc.contributor.author","Welpinghus, Henrike"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Ghezzi, Pietro"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Erythropoietin (EPO) reduces symptoms of experimental autoimmune encephalomyelitis in rodents and shows neuroregenerative effects in chronic progressive multiple sclerosis. The mechanisms of action of EPO in these conditions with shared immunological etiology are still unclear. Therefore, we used a model of toxic demyelination allowing exclusion of T cell-mediated inflammation. In a double-blind (for food/injections), placebo-controlled, longitudinal four-arm design, 8-wk-old C57BL/6 mice (n = 26/group) were assigned to cuprizone-containing (0.2%) or regular food (ground chow) for 6 wks. After 3 wks, mice were injected every other day with placebo or EPO (5,000 IU/kg intraperitoneally) until the end of cuprizone feeding. Half of the mice were exposed to behavioral testing, magnetic resonance imaging (MRI) and histology immediately after treatment cessation, whereas the other half were allowed a 3-wk treatment-free recovery. Immediately after termination of cuprizone feeding, all toxin-exposed mice were compromised regarding vestibulomotor function/coordination, with EPO-treated animals performing better than placebo. Likewise, ventricular enlargement after cuprizone, as documented by MRI, was less pronounced upon EPO. After a 3-wk recovery, remarkable spontaneous improvement was observed in all mice with no measurable further benefit in the EPO group (\"ceiling effect\"). Histological analysis of the corpus callosum revealed attenuation by EPO of the cuprizone-induced increase in microglial numbers and amyloid precursor protein accumulations as a readout of inflammation and axonal degeneration. To conclude, EPO ameliorates neurological symptoms in the cuprizone model of demyelination, possibly by reduction of inflammation-associated axonal degeneration in white matter tracts. These findings underscore the value of future therapeutic strategies for multiple sclerosis based on EPO or EPO variants."],["dc.identifier.doi","10.2119/molmed.2011.00457"],["dc.identifier.gro","3150534"],["dc.identifier.pmid","22396019"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7306"],["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","Erythropoietin attenuates neurological and histological consequences of toxic demyelination in mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","480"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","489"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Kämmer, Daniel"],["dc.contributor.author","Riechers, Claas-Christian"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Price, Jack"],["dc.contributor.author","Meyer, Barbara"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:33Z"],["dc.date.available","2017-09-07T11:45:33Z"],["dc.date.issued","2006"],["dc.description.abstract","In humans, neurotrauma is suspected to cause brain atrophy and accelerate slowly progressive neurodegenerative disorders, such as Alzheimer's disease or schizophrenia. However, a direct link between brain injury and subsequent delayed global neurodegeneration has remained elusive. Here we show that juvenile (4-week-old) mice that are given a discrete unilateral lesion of the parietal cortex, develop to adulthood without obvious clinical symptoms. However, when monitored 3 and 9 months after lesioning, using high-resolution three-dimensional MRI and behavioural testing, the same mice display global neurodegenerative changes. Surprisingly, erythropoietin, a haematopoietic growth factor with potent neuroprotective activity, prevents behavioural abnormalities, cognitive dysfunction and brain atrophy when given for 2 weeks after acute brain injury. This demonstrates that a localized brain lesion is a primary cause of delayed global neurodegeneration that can be efficiently counteracted by neuroprotection."],["dc.identifier.doi","10.1093/brain/awh703"],["dc.identifier.doi","10.1093/brain/awh703"],["dc.identifier.gro","3150392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7151"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0006-8950"],["dc.subject","EPO; MRI; neuroprotection; neurodegeneration; neurotrauma; schizophrenia"],["dc.title","Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["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","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","1752"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1767"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Ott, C."],["dc.contributor.author","Wüstefeld, L."],["dc.contributor.author","Offen, N."],["dc.contributor.author","Neher, R. A."],["dc.contributor.author","Mitkovski, M."],["dc.contributor.author","Winkler, D."],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Fries, L."],["dc.contributor.author","Goebbels, S."],["dc.contributor.author","Vreja, I. C."],["dc.contributor.author","Hagemeyer, N."],["dc.contributor.author","Dittrich, M."],["dc.contributor.author","Rossetti, M. F."],["dc.contributor.author","Kröhnert, K."],["dc.contributor.author","Hannke, K."],["dc.contributor.author","Boretius, S."],["dc.contributor.author","Zeug, A."],["dc.contributor.author","Höschen, C."],["dc.contributor.author","Dandekar, T."],["dc.contributor.author","Dere, E."],["dc.contributor.author","Neher, E."],["dc.contributor.author","Rizzoli, S. O."],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:53:29Z"],["dc.date.available","2017-09-07T11:53:29Z"],["dc.date.issued","2016"],["dc.description.abstract","Recombinant human erythropoietin (EPO) improves cognitive performance in neuropsychiatric diseases ranging from schizophrenia and multiple sclerosis to major depression and bipolar disease. This consistent EPO effect on cognition is independent of its role in hematopoiesis. The cellular mechanisms of action in brain, however, have remained unclear. Here we studied healthy young mice and observed that 3-week EPO administration was associated with an increased number of pyramidal neurons and oligodendrocytes in the hippocampus of ~20%. Under constant cognitive challenge, neuron numbers remained elevated until >6 months of age. Surprisingly, this increase occurred in absence of altered cell proliferation or apoptosis. After feeding a 15N-leucine diet, we used nanoscopic secondary ion mass spectrometry, and found that in EPO-treated mice, an equivalent number of neurons was defined by elevated 15N-leucine incorporation. In EPO-treated NG2-Cre-ERT2 mice, we confirmed enhanced differentiation of preexisting oligodendrocyte precursors in the absence of elevated DNA synthesis. A corresponding analysis of the neuronal lineage awaits the identification of suitable neuronal markers. In cultured neurospheres, EPO reduced Sox9 and stimulated miR124, associated with advanced neuronal differentiation. We are discussing a resulting working model in which EPO drives the differentiation of non-dividing precursors in both (NG2+) oligodendroglial and neuronal lineages. As endogenous EPO expression is induced by brain injury, such a mechanism of adult neurogenesis may be relevant for central nervous system regeneration."],["dc.identifier.doi","10.1038/mp.2015.212"],["dc.identifier.fs","620695"],["dc.identifier.gro","3145088"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14225"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2785"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1359-4184"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Revisiting adult neurogenesis and the role of erythropoietin for neuronal and oligodendroglial differentiation in the hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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.firstpage","2025"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","2040"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Moschny, Nicole"],["dc.contributor.author","Baudewig, Jürgen"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2016"],["dc.description.abstract","Subtle white matter abnormalities have emerged as a hallmark of brain alterations in magnetic resonance imaging or upon autopsy of mentally ill subjects. However, it is unknown whether such reduction of white matter and myelin contributes to any disease-relevant phenotype or simply constitutes an epiphenomenon, possibly even treatment-related. Here, we have re-analyzed Mbp heterozygous mice, the unaffected parental strain of shiverer, a classical neurological mutant. Between 2 and 20 months of age, Mbp+/- versus Mbp+/+ littermates were deeply phenotyped by combining extensive behavioral/cognitive testing with MRI, 1H-MR spectroscopy, electron microscopy, and molecular techniques. Surprisingly, Mbp-dependent myelination was significantly reduced in the prefrontal cortex. We also noticed a mild but progressive hypomyelination of the prefrontal corpus callosum and low-grade inflammation. While most behavioral functions were preserved, Mbp+/- mice exhibited defects of sensorimotor gating, as evidenced by reduced prepulse-inhibition, and a late-onset catatonia phenotype. Thus, subtle but primary abnormalities of CNS myelin can be the cause of a persistent cortical network dysfunction including catatonia, features typical of neuropsychiatric conditions."],["dc.identifier.doi","10.1002/glia.23039"],["dc.identifier.gro","3150347"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7101"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Cortical network dysfunction caused by a subtle defect of myelination"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","734"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","745"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Balmuth, Evan"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Hertel, Johannes"],["dc.contributor.author","Habes, Mohamad"],["dc.contributor.author","Bittner, Robert A."],["dc.contributor.author","Pan, Hong"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Langner, Sönke"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Kittel-Schneider, Sarah"],["dc.contributor.author","Homuth, Georg"],["dc.contributor.author","Davatzikos, Christos"],["dc.contributor.author","Völzke, Henry"],["dc.contributor.author","West, Brian L."],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Grabe, Hans Jörgen"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2020-12-10T18:38:19Z"],["dc.date.available","2020-12-10T18:38:19Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1172/JCI97032"],["dc.identifier.eissn","1558-8238"],["dc.identifier.issn","0021-9738"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77272"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Microglia ablation alleviates myelin-associated catatonic signs in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]