Stadelmann-Nessler, Christine

[["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T08:39:40Z"],["dc.date.available","2018-11-07T08:39:40Z"],["dc.date.issued","2010"],["dc.format.extent","657"],["dc.identifier.isi","000293331101589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19052"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Geneva, SWITZERLAND"],["dc.relation.issn","1351-5101"],["dc.title","Comparative study of neuronal and axonal pathology in early multiple sclerosis and CNS trauma lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Juergens, T."],["dc.contributor.author","Glaser, Raoul"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T11:25:14Z"],["dc.date.available","2018-11-07T11:25:14Z"],["dc.date.issued","2009"],["dc.format.extent","S180"],["dc.identifier.isi","000269652500538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56580"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","Propagation of cortical spreading depression inversely correlates with cortical myelin content"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1972"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1983"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Ernsting, Tristan"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:27:12Z"],["dc.date.available","2018-11-07T09:27:12Z"],["dc.date.issued","2006"],["dc.description.abstract","Recent studies have revealed widespread demyelination in the cortex of patients with chronic multiple sclerosis. In contrast to white matter lesions, cortical multiple sclerosis lesions are accompanied by only minor inflammation. Research into the pathogenesis of cortical lesion formation has been hampered by the fact that the conventional rodent model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), does not regularly affect the cortex. To overcome this limitation we developed a new rat model of cortical multiple sclerosis. Lesions were stereotactically targeted to the cerebral cortex by injection of pro-inflammatory mediators in animals that were immunized subclinically with myelin oligodendrocyte glycoprotein (MOG). We thus generated highly reproducible demyelinated lesions in the neocortex with remarkable histological similarities to cortical multiple sclerosis lesions. The focal cortical EAE model led to the typical pattern of intracortical and subpial demyelination, infiltration with inflammatory cells, complement deposition, acute axonal damage and neuronal cell death. Surprisingly, extensive cortical inflammation largely resolved within 2 weeks. Furthermore, cortical demyelination was readily compensated by rapid remyelination. Our data thus suggest that cortical inflammation is a transient phenomenon, and that remyelination of cortical inflammatory-demyelinating lesions may occur rapidly."],["dc.identifier.doi","10.1093/brain/awl135"],["dc.identifier.isi","000239900600007"],["dc.identifier.pmid","16714315"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30479"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","A new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Garea-Rodriguez, Enrique"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Merkler, Doron"],["dc.date.accessioned","2018-11-07T11:11:01Z"],["dc.date.available","2018-11-07T11:11:01Z"],["dc.date.issued","2008"],["dc.format.extent","343"],["dc.identifier.isi","000258235200026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53335"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","53rd Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Wurzburg, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Effect of repeated inflammatory demyelination on intrinsic remyelination in the targeted cortical EAE model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","eaav5519"],["dc.bibliographiccitation.issue","498"],["dc.bibliographiccitation.journal","Science Translational Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Steinbach, Karin"],["dc.contributor.author","Vincenti, Ilena"],["dc.contributor.author","Egervari, Kristof"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Page, Nicolas"],["dc.contributor.author","Klimek, Bogna"],["dc.contributor.author","Rossitto-Borlat, Irène"],["dc.contributor.author","Di Liberto, Giovanni"],["dc.contributor.author","Muschaweckh, Andreas"],["dc.contributor.author","Wagner, Ingrid"],["dc.contributor.author","Hammad, Karim"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Korn, Thomas"],["dc.contributor.author","Hartley, Oliver"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.contributor.author","Merkler, Doron"],["dc.date.accessioned","2020-12-10T18:36:47Z"],["dc.date.available","2020-12-10T18:36:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1126/scitranslmed.aav5519"],["dc.identifier.eissn","1946-6242"],["dc.identifier.issn","1946-6234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76737"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Brain-resident memory T cells generated early in life predispose to autoimmune disease in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","369"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","374"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Schmelting, Barthel"],["dc.contributor.author","Czeh, Boldizsar"],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:30:14Z"],["dc.date.available","2018-11-07T09:30:14Z"],["dc.date.issued","2006"],["dc.description.abstract","Pathomorphological studies described pathological heterogeneity in patients with multiple sclerosis (MS). Different effector mechanisms might therefore be responsible for lesion formation in MS. The present report shows that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in common marmoset monkeys reflects one specific lesional subtype of MS, namely MS pattern 11 lesions with antibody/complement-mediated damage. MOG-induced EAE in marmoset monkeys will, therefore, provide an ideal model for therapeutic approaches directed against B-cell/antibody/complement in MS."],["dc.identifier.doi","10.1191/1352458506ms1290oa"],["dc.identifier.isi","000239431200002"],["dc.identifier.pmid","16900750"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31257"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.title","Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in the common marmoset reflects the immunopathology of pattern II multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","163"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","171"],["dc.bibliographiccitation.volume","193"],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Boger, I."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:54:30Z"],["dc.date.available","2017-09-07T11:54:30Z"],["dc.date.issued","2005"],["dc.description.abstract","In patients with multiple sclerosis (MS), non-remitting deficits are mainly caused by axonal and neuronal damage. We demonstrated previously that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis in rats provokes severe axonal and neuronal injury even before clinical manifestation of the disease. In our present study, we investigated effects of simvastatin treatment on degeneration of retinal ganglion cell (RGC) bodies as well as their axons during MOG-induced optic neuritis. Electrophysiological functions of optic nerves and RGCs were analyzed in vivo. Although neuroprotective effects of simvastatin have been demonstrated before in other experimental settings, we did not observe an increase in RGC survival nor an improvement of visual functions. As we could not reproduce the anti-inflammatory effects that were observed under statin therapy in other EAE models, we hypothesize that patients suffering from optic neuritis might not take advantage of simvastatin applications. (c) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2004.12.010"],["dc.identifier.gro","3143859"],["dc.identifier.isi","000228413300016"],["dc.identifier.pmid","15817275"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1419"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Simvastatin treatment does not protect retinal ganglion cells from degeneration in a rat model of autoimmune optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Bittner, A."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Sommer, N."],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T10:56:29Z"],["dc.date.available","2018-11-07T10:56:29Z"],["dc.date.issued","2005"],["dc.identifier.isi","000232249900170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50022"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hodder Arnold, Hodder Headline Plc"],["dc.publisher.place","London"],["dc.relation.conference","21st Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis/10th Annual Meeting of Rehabilitation in MS"],["dc.relation.eventlocation","Thessaloniki, GREECE"],["dc.title","MRI-histopathology correlation in a clonal mouse EAE model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","375"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","385"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:45:35Z"],["dc.date.available","2017-09-07T11:45:35Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurodegenerative processes determine the clinical disease course of multiple sclerosis, an inflammatory autoimmune CNS disease that frequently manifests with acute optic neuritis. None of the established multiple sclerosis therapies has been shown to clearly reduce neurodegeneration. In a rat model of experimental autoimmune encephalomyelitis, we recently demonstrated increased neuronal apoptosis under methylprednisolone therapy, although CNS inflammation was effectively controlled. In the present study, we combined steroid treatment with application of erythropoietin to target inflammatory as well as neurodegenerative aspects. After immunization with myelin oligodendrocyte glycoprotein (MOG), animals were randomly assigned to six treatment groups receiving different combinations of erythropoietin and methylprednisolone, or respective monotherapies. After MOG-induced experimental autoimmune encephalomyelitis became clinically manifest, optic neuritis was monitored by recording visual evoked potentials. The function of retinal ganglion cells, the neurons that form the axons of the optic nerve, was measured by electroretinograms. Functional and histo pathological data of retinal ganglion cells and optic nerves revealed that neuron and axon protection was most effective when erythropoietin treatment that was started at immunization was combined with high-dose methylprednisolone therapy given from days 1 to 3 of MOG-induced experimental autoimmune encephalomyelitis. In contrast, isolated neuronal or axonal protection without clinical benefit was achieved under monotherapy with erythropoietin or methylprednisolone, respectively."],["dc.identifier.doi","10.1093/brain/awh365"],["dc.identifier.gro","3150407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7168"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.doi","10.1093/brain/awh365"],["dc.relation.issn","0006-8950"],["dc.title","Combined therapy with methylprednisolone and erythropoietin in a model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:30:54Z"],["dc.date.available","2018-11-07T09:30:54Z"],["dc.date.issued","2013"],["dc.description.abstract","The extent of irreversible neuroaxonal damage is the key determinant of permanent disability in traumatic and inflammatory conditions of the central nervous system (CNS). Structural damage is nevertheless in part compensated by neuroplastic events. However, it is unknown whether the same kinetics and mechanisms of neuroaxonal de- and regeneration take place in inflammatory and traumatic conditions. We analyzed neuroaxonal degeneration and plasticity in early multiple sclerosis (MS) lesions and traumatic brain injury (TBI). Neuroaxonal degeneration identified by the presence of SMI31+ chromatolytic neurons and SMI32+ axonal profiles were characteristic features of leukocortical TBI lesions. Axonal transport disturbances as determined by amyloid precursor protein (APP)+ spheroids were present in both TBI and MS lesions to a similar degree. Neurons expressing growth-associated protein 43 (GAP43) and synaptophysin (Syn) were found under both pathological conditions. However, axonal swellings immunopositive for GAP43 and Syn clearly prevailed in subcortical MS lesions, suggesting a higher regenerative potential in MS. In this context, GAP43+/APP+ axonal spheroid ratios correlated with macrophage infiltration in TBI and MS lesions, supporting the idea that phagocyte activation might promote neuroplastic events. Furthermore, axonal GAP43+ and Syn+ swellings correlated with prolonged survival after TBI, indicating a sustained regenerative response."],["dc.description.sponsorship","DFG transregional collaborative research center 43; DFG [GRK 632]"],["dc.identifier.doi","10.1111/j.1750-3639.2012.00608.x"],["dc.identifier.isi","000312248600002"],["dc.identifier.pmid","22612622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31420"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1015-6305"],["dc.title","Neuroaxonal Regeneration is More Pronounced in Early Multiple Sclerosis than in Traumatic Brain Injury Lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]