Ott, Christoph

[["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","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Saschenbrecker, Sandra"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Borowski, Kathrin"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Lemke, Sandra"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Wienands, Jürgen"],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Stöcker, Winfried"],["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","ObjectiveWe previously reported an unexpectedly high seroprevalence (∼10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoantibodies (AB) in healthy and neuropsychiatrically ill subjects (N = 2,817). This finding challenges an unambiguous causal relationship of serum AB with brain disease. To test whether similar results would be obtained for other brain antigen-directed AB previously connected with pathological conditions, we systematically screened serum samples of 4,236 individuals.MethodsSerum samples of healthy (n = 1,703) versus neuropsychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrophic lateral sclerosis, personality disorder; total n = 2,533) were tested. For analysis based on indirect immunofluorescence, we used biochip mosaics of frozen brain sections (rat, monkey) and transfected HEK293 cells expressing respective recombinant target antigens.ResultsSeroprevalence of all screened AB was comparable in healthy and ill individuals. None of them, however, reached the abundance of NMDAR1 AB (again ∼10%; immunoglobulin [Ig] G ∼1%). Appreciable frequency was noted for AB against amphiphysin (2.0%), ARHGAP26 (1.3%), CASPR2 (0.9%), MOG (0.8%), GAD65 (0.5%), Ma2 (0.5%), Yo (0.4%), and Ma1 (0.4%), with titers and Ig class distribution similar among groups. All other AB were found in ≤0.1% of individuals (anti–AMPAR-1/2, AQP4, CV2, Tr/DNER, DPPX-IF1, GABAR-B1/B2, GAD67, GLRA1b, GRM1, GRM5, Hu, LGl1, recoverin, Ri, ZIC4). The predominant Ig class depended on antigen location, with intracellular epitopes predisposing to IgG (chi-square = 218.91, p = 2.8 × 10−48).InterpretationTo conclude, the brain antigen-directed AB tested here are comparably detectable in healthy subjects and the disease groups studied here, thus questioning an upfront pathological role of these serum AB."],["dc.identifier.doi","10.1002/ana.24189"],["dc.identifier.gro","3150539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7312"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Seroprevalence of autoantibodies against brain antigens in health and disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","803"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","815"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Oliveira, Bárbara"],["dc.contributor.author","Erck, Christian"],["dc.contributor.author","Zafiriou, Maria Patapia"],["dc.contributor.author","Peteri, Ulla-Kaisa"],["dc.contributor.author","Hesse, Dörte"],["dc.contributor.author","Gerhart, Simone"],["dc.contributor.author","Altas, Bekir"],["dc.contributor.author","Kolbow, Tekla"],["dc.contributor.author","Stadler, Herbert"],["dc.contributor.author","Kawabe, Hiroshi"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Schulz-Schaeffer, Walter"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2015"],["dc.description.abstract","Erythropoietin (EPO) exerts potent neuroprotective, neuroregenerative and procognitive functions. However, unequivocal demonstrationof erythropoietin receptor (EPOR) expression in brain cells has remained difficult since previously available anti-EPORantibodies (EPOR-AB) were unspecific. We report here a new, highly specific, polyclonal rabbit EPOR-AB directed against differentepitopes in the cytoplasmic tail of human and murine EPOR and its characterization by mass spectrometric analysis of immunoprecipitatedendogenous EPOR, Western blotting, immunostaining and flow cytometry. Among others, we applied genetic strategiesincluding overexpression, Lentivirus-mediated conditional knockout of EpoR and tagged proteins, both on cultured cellsand tissue sections, as well as intracortical implantation of EPOR-transduced cells to verify specificity. We show examples of EPORexpression in neurons, oligodendroglia, astrocytes and microglia. Employing this new EPOR-AB with double-labeling strategies, wedemonstrate membrane expression of EPOR as well as its localization in intracellular compartments such as the Golgi apparatus.Moreover, we show injury-induced expression of EPOR. In mice, a stereotactically applied stab wound to the motor cortex leadsto distinct EpoR expression by reactive GFAP-expressing cells in the lesion vicinity. In a patient suffering from epilepsy, neurons andoligodendrocytes of the hippocampus strongly express EPOR. To conclude, this new analytical tool will allow neuroscientists to pinpointEPOR expression in cells of the nervous system and to better understand its role in healthy conditions, including brain development,as well as under pathological circumstances, such as upregulation upon distress and injury."],["dc.identifier.doi","10.2119/molmed.2015.00192"],["dc.identifier.gro","3150554"],["dc.identifier.pmid","26349059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7328"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/321"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.haserratum","/handle/2/84392"],["dc.relation.issn","1076-1551"],["dc.title","Widespread expression of erythropoietin receptor in brain and its induction by injury"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]