Boretius, Susann

[["dc.bibliographiccitation.firstpage","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Tuoc, Tran Cong"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Sansom, Stephen N."],["dc.contributor.author","Pitulescu, Mara-Elena"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Livesey, Frederick J."],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2017-09-07T11:44:52Z"],["dc.date.available","2017-09-07T11:44:52Z"],["dc.date.issued","2013"],["dc.description.abstract","Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 overexpression results in the opposite phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting euchromatin structure and thereby modulating the binding efficiency of the Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture."],["dc.identifier.doi","10.1016/j.devcel.2013.04.005"],["dc.identifier.gro","3150356"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7111"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1534-5807"],["dc.title","Chromatin Regulation by BAF170 Controls Cerebral Cortical Size and Thickness"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","735"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","744"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Wozny, Christian"],["dc.contributor.author","Breustedt, Jörg"],["dc.contributor.author","Wolk, Friederike"],["dc.contributor.author","Varoqueaux, Frédérique"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Zivkovic, Aleksandar R."],["dc.contributor.author","Neeb, Antje"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Schmitz, Dietmar"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ivanovic, Aleksandra"],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2009"],["dc.description.abstract","AMPA-type glutamate receptors mediate fast excitatory synaptic transmission in the vertebrate brain. Their surface expression at synapses between neurons is regulated in an activity-dependent and activity-independent manner. The protein machinery that regulates synaptic targeting, anchoring and turnover of AMPA receptors consists of several types of specialized scaffolding proteins. The FERM domain scaffolding proteins 4.1G and 4.1N were previously suggested to act jointly in binding and regulating synaptic trafficking of the AMPA receptor subunits GluR1 and GluR4. To determine the functions of 4.1G and 4.1N in vivo, we generated a mutant mouse line that lacks 4.1G entirely and expresses 4.1N at 22% of wild-type levels. These mice had combined 4.1G and 4.1N protein expression in the hippocampus at 12% of wild-type levels (equivalent to 8-10% of combined GluR1 and GluR4 expression levels). They show a moderate reduction in synaptosomal expression levels of the AMPA receptor subunit GluR1 at 3 weeks of age, but no change in basic glutamatergic synaptic transmission and long-term potentiation in the hippocampus. Our study indicates that 4.1G and 4.1N do not have a crucial role in glutamatergic synaptic transmission and the induction and maintenance of long-term plastic changes in synaptic efficacy."],["dc.identifier.doi","10.1242/jcs.037382"],["dc.identifier.gro","3150376"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7134"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0021-9533"],["dc.subject","Knockout; Mouse; Hippocampus; GluR1; GluR4; Synaptic plasticity"],["dc.title","The function of glutamatergic synapses is not perturbed by severe knockdown of 4.1N and 4.1G expression"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","209"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Magnetic Resonance Imaging"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Michaelis, Thomas"],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2006"],["dc.description.abstract","This magnetic resonance imaging (MRI) study describes mapping of the habenulo-interpeduncular pathway in living mice based on manganese-induced contrast. Six hours after intracerebroventricular microinjection of MnCl2, T1-weighted 3D MRI (2.35 T) at 117 μm isotropic resolution revealed a continuous pattern of anterograde labeling from the habenula via the fasciculus retroflexus to the interpeduncular nucleus. Alternatively, the less invasive systemic administration of MnCl2 allowed for monitoring of the dynamic uptake pattern of respective neural components with even higher reproducibility across animals. Time courses covered the range from 42 min to 24 h after injection. In conclusion, manganese-enhanced MRI may open new ways for functional assessments of the habenulo-interpeduncular system in animal models with cognitive impairment."],["dc.identifier.doi","10.1016/j.mri.2005.10.034"],["dc.identifier.gro","3150377"],["dc.identifier.pmid","16563949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7135"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0730-725X"],["dc.subject","Habenula; Magnetic resonance imaging; Manganese; Mice; Neural pathways"],["dc.title","Mapping of the habenulo-interpeduncular pathway in living mice using manganese-enhanced 3D MRI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","596"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","602"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Watanabe, Takashi"],["dc.contributor.author","Natt, Oliver"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Utz, Sandra"],["dc.contributor.author","Schachtner, Joachim"],["dc.date.accessioned","2017-09-07T11:45:31Z"],["dc.date.available","2017-09-07T11:45:31Z"],["dc.date.issued","2005"],["dc.description.abstract","High-resolution 3D MRI of male pupae of Manduca sexta was performed at 2.35 T in order to evaluate its potential for an in vivo characterization of insect brain during metamorphosis. T1-weighted 3D FLASH (TR/TE = 20/7.8 ms, 25° flip angle) and T2-weighted 3D fast SE MRI data sets (TR/TEeff = 3000/100 ms) were acquired at different developmental stages with an isotropic resolution of 100 μm. Both T1- and T2-weighted 3D MRI allowed for the identification of cerebral structures such as the antennal nerve, antennal and optical lobe, and central brain. Pronounced developmental alterations of the morphology were observed during metamorphosis. The results demonstrate the feasibility of 3D MRI at nanoliter resolution to identify major brain systems of M. sexta and respective changes during pupal development from caterpillar to sphinx moth. Together with the use of suitable contrast agents, this approach may provide new ways for studying the axonal connectivity and neural function of the developing insect brain."],["dc.identifier.doi","10.1016/j.neuroimage.2004.08.048"],["dc.identifier.gro","3150381"],["dc.identifier.pmid","15627604"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7139"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1053-8119"],["dc.subject","Magnetic resonance imaging; Metamorphosis; Brain development; Manduca sexta; Entomology"],["dc.title","In vivo 3D MRI of insect brain: cerebral development during metamorphosis of Manduca sexta"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2678"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","2688"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Escher, Angelika"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2011"],["dc.description.abstract","Magnetic resonance imaging (MRI) is the gold standard for the detection of multiple sclerosis (MS) lesions. However, current MRI techniques provide little information about the structural features of a brain lesion with inflammatory cell infiltration, demyelination, gliosis, acute axonal damage and axonal loss. To identify methods for a differentiation of demyelination, inflammation, and axonal damage we developed a novel mouse model combining cuprizone-induced demyelination and experimental autoimmune encephalomyelitis. MS-like brain lesions were assessed by T1-weighted, T2-weighted, and magnetization transfer MRI as well as by diffusion tensor imaging (DTI). T2-weighted MRI differentiated control and diseased mice, while T1-weighted MRI better reflected the extent of inflammation and axonal damage. In DTI, axonal damage and cellular infiltration led to a reduction of the axial diffusivity, whereas primary demyelination after cuprizone treatment was reflected by changes in radial but not axial diffusivity. Importantly, alterations in radial diffusivity were less pronounced in mice with demyelination, inflammation, and acute axonal damage, indicating that radial diffusivity may underestimate demyelination in acute MS lesions. In conclusion, the combined information from different DTI parameters allows for a more precise identification of solely demyelinated lesions versus demyelinated and acutely inflamed lesions. These findings are of relevance for offering individualized, stage-adapted therapies for MS patients."],["dc.identifier.doi","10.1016/j.neuroimage.2011.08.051"],["dc.identifier.gro","3150360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7115"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1053-8119"],["dc.title","Assessment of lesion pathology in a new animal model of MS by multiparametric MRI and DTI"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["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.artnumber","e0168174"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Huhndorf, Monika"],["dc.contributor.author","Moussavi, Amir"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Will, Olga Maria"],["dc.contributor.author","Hattermann, Kirsten"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Jansen, Olav"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.editor","Sherman, Jonathan H."],["dc.date.accessioned","2017-09-07T11:44:48Z"],["dc.date.available","2017-09-07T11:44:48Z"],["dc.date.issued","2017"],["dc.description.abstract","ObjectivesAngiogenesis and anti-angiogenetic medications play an important role in progression and therapy of glioblastoma. In this context, in vivo characterization of the blood-brain-barrier and tumor vascularization may be important for individual prognosis and therapy optimization.MethodsWe analyzed perfusion and capillary permeability of C6-gliomas in rats at different stages of tumor-growth by contrast enhanced MRI and dynamic susceptibility contrast (DSC) MRI at 7 Tesla. The analyses included maps of relative cerebral blood volume (CBV) and signal recovery derived from DSC data over a time period of up to 35 days after tumor cell injections.ResultsIn all rats tumor progression was accompanied by temporal and spatial changes in CBV and capillary permeability. A leakage of the blood-brain barrier (slow contrast enhancement) was observed as soon as the tumor became detectable on T2-weighted images. Interestingly, areas of strong capillary permeability (fast signal enhancement) were predominantly localized in the center of the tumor. In contrast, the tumor rim was dominated by an increased CBV and showed the highest vessel density compared to the tumor center and the contralateral hemisphere as confirmed by histology.ConclusionSubstantial regional differences in the tumor highlight the importance of parameter maps in contrast or in addition to region-of-interest analyses. The data vividly illustrate how MRI including contrast-enhanced and DSC-MRI may contribute to a better understanding of tumor development."],["dc.identifier.doi","10.1371/journal.pone.0168174"],["dc.identifier.gro","3150343"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7096"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Alterations of the Blood-Brain Barrier and Regional Perfusion in Tumor Development: MRI Insights from a Rat C6 Glioma Model"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["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","213"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Medical Primatology"],["dc.bibliographiccitation.lastpage","218"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Abaei, A."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Tammer, Roland"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Schlumbohm, C."],["dc.contributor.author","Fuchs, E."],["dc.date.accessioned","2017-09-07T11:45:28Z"],["dc.date.available","2017-09-07T11:45:28Z"],["dc.date.issued","2009"],["dc.description.abstract","BACKGROUND: Animal models of human brain disorders often have to rely on non-human primates because of their immunological, physiological, and cognitive similarities to humans. METHODS: Localized proton magnetic resonance spectroscopy was performed to assess cerebral metabolite profiles of male common marmoset monkeys in vivo and to determine putative alterations of adult brain metabolism in response to intrauterine hyperexposure to the synthetic glucocorticoid hormone dexamethasone. RESULTS: Excellent spectral quality allowed for absolute quantification of the concentrations of major metabolites in predominantly white matter, gray matter, and thalamus. Marmoset monkeys intrauterinely hyperexposed to dexamethasone revealed normal neurochemical profiles at adulthood. CONCLUSIONS: Prenatally applied dexamethasone does not lead to persistent metabolic alterations affecting adult brain integrity."],["dc.identifier.doi","10.1111/j.1600-0684.2009.00342.x"],["dc.identifier.gro","3150368"],["dc.identifier.pmid","19374665"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7125"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0047-2565"],["dc.subject","Brain metabolism; Callithrix jacchus; glucocorticoids; prenatal; preterm birth; proton magnetic resonance spectroscopy"],["dc.title","Intrauterine hyperexposure to dexamethasone of the common marmoset monkey revealed normal cerebral metabolite concentrations in adulthood as assessed by quantitative proton magnetic resonance spectroscopy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]