Merkler, Doron

[["dc.bibliographiccitation.artnumber","13275"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Mezydlo, Aleksandra"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Potz, Stephanie"],["dc.contributor.author","Meinl, Edgar"],["dc.contributor.author","Matznick, Florian E. H."],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Ghanem, Alexander"],["dc.contributor.author","Conzelmann, Karl-Klaus"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Routh, Matthew"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T10:05:43Z"],["dc.date.available","2018-11-07T10:05:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocyte damage is a central event in the pathogenesis of the common neuro-inflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge."],["dc.identifier.doi","10.1038/ncomms13275"],["dc.identifier.isi","000387837900001"],["dc.identifier.pmid","27848954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","U135"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Sorbara, Catherine"],["dc.contributor.author","Brinkoetter, Mary"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Bareyre, Florence Martine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T08:57:32Z"],["dc.date.available","2018-11-07T08:57:32Z"],["dc.date.issued","2011"],["dc.description.abstract","In multiple sclerosis, a common inflammatory disease of the central nervous system, immune-mediated axon damage is responsible for permanent neurological deficits(1,2). How axon damage is initiated is not known. Here we use in vivo imaging to identify a previously undescribed variant of axon damage in a mouse model of multiple sclerosis. This process, termed 'focal axonal degeneration' (FAD), is characterized by sequential stages, beginning with focal swellings and progressing to axon fragmentation. Notably, most swollen axons persist unchanged for several days, and some recover spontaneously. Early stages of FAD can be observed in axons with intact myelin sheaths. Thus, contrary to the classical view(2-6), demyelination-a hallmark of multiple sclerosis-is not a prerequisite for axon damage. Instead, focal intra-axonal mitochondrial pathology is the earliest ultrastructural sign of damage, and it precedes changes in axon morphology. Molecular imaging and pharmacological experiments show that macrophage-derived reactive oxygen and nitrogen species (ROS and RNS) can trigger mitochondrial pathology and initiate FAD. Indeed, neutralization of ROS and RNS rescues axons that have already entered the degenerative process. Finally, axonal changes consistent with FAD can be detected in acute human multiple sclerosis lesions. In summary, our data suggest that inflammatory axon damage might be spontaneously reversible and thus a potential target for therapy."],["dc.identifier.doi","10.1038/nm.2324"],["dc.identifier.isi","000289245100041"],["dc.identifier.pmid","21441916"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23423"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis"],["dc.type","journal_article"],["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","46"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","57"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Lalive, Patrice H."],["dc.contributor.author","Benkhoucha, Mahdia"],["dc.contributor.author","Ngoc Lan Tran, Ngoc Lan Tran"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Santiago-Raber, Marie-Laure"],["dc.date.accessioned","2018-11-07T09:46:42Z"],["dc.date.available","2018-11-07T09:46:42Z"],["dc.date.issued","2014"],["dc.identifier.isi","000330803400007"],["dc.identifier.pmid","24018482"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34941"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","TLR7 signaling exacerbates CNS autoimmunity through downregulation of Foxp3(+) Treg cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2087"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Experimental Medicine"],["dc.bibliographiccitation.lastpage","2103"],["dc.bibliographiccitation.volume","210"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Bergthaler, Andreas"],["dc.contributor.author","Fernandez, Marylise"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Steinbach, Karin"],["dc.contributor.author","Vorm, Mariann"],["dc.contributor.author","Coras, Roland"],["dc.contributor.author","Bluemcke, Ingmar"],["dc.contributor.author","Bonilla, Weldy V."],["dc.contributor.author","Fleige, Anne"],["dc.contributor.author","Forman, Ruth"],["dc.contributor.author","Mueller, Werner"],["dc.contributor.author","Becher, Burkhard"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.contributor.author","Merkler, Doron"],["dc.date.accessioned","2018-11-07T09:19:48Z"],["dc.date.available","2018-11-07T09:19:48Z"],["dc.date.issued","2013"],["dc.description.abstract","Neurons are postmitotic and thus irreplaceable cells of the central nervous system (CNS). Accordingly, CNS inflammation with resulting neuronal damage can have devastating consequences. We investigated molecular mediators and structural consequences of CD8(+) T lymphocyte (CTL) attack on neurons in vivo. In a viral encephalitis model in mice, disease depended on CTL-derived interferon-gamma (IFN-gamma) and neuronal IFN-gamma signaling. Downstream STAT1 phosphorylation and nuclear translocation in neurons were associated with dendrite and synapse loss (deafferentation). Analogous molecular and structural alterations were also found in human Rasmussen encephalitis, a CTL-mediated human autoimmune disorder of the CNS. Importantly, therapeutic intervention by IFN-gamma blocking antibody prevented neuronal deafferentation and clinical disease without reducing CTL responses or CNS infiltration. These findings identify neuronal IFN-gamma signaling as a novel target for neuroprotective interventions in CTL-mediated CNS disease."],["dc.identifier.doi","10.1084/jem.20122143"],["dc.identifier.isi","000324813000016"],["dc.identifier.pmid","23999498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28728"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Rockefeller Univ Press"],["dc.relation.issn","0022-1007"],["dc.title","Neuroprotective intervention by interferon-gamma blockade prevents CD8(+) T cell-mediated dendrite and synapse loss"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e22735"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Ghosh, Aniket"],["dc.contributor.author","Manrique-Hoyos, Natalia"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T08:54:12Z"],["dc.date.available","2018-11-07T08:54:12Z"],["dc.date.issued","2011"],["dc.description.abstract","Glial dysfunction has been implicated in a number of neurodegenerative diseases. In this study we investigated the consequences of glial and oligodendrocyte ablation on neuronal integrity and survival in Drosophila and adult mice, respectively. Targeted genetic ablation of glia was achieved in the adult Drosophila nervous system using the GAL80-GAL4 system. In mice, oligodendrocytes were depleted by the injection of diphtheria toxin in MOGi-Cre/iDTR double transgenic animals. Acute depletion of oligodendrocytes induced axonal injury, but did not cause neuronal cell death in mice. Ablation of glia in adult flies triggered neuronal apoptosis and resulted in a marked reduction in motor performance and lifespan. Our study shows that the targeted depletion of glia triggers secondary neurotoxicity and underscores the central contribution of glia to neuronal homeostasis. The models used in this study provide valuable systems for the investigation of therapeutic strategies to prevent axonal or neuronal damage."],["dc.description.sponsorship","ERC [204034]"],["dc.identifier.doi","10.1371/journal.pone.0022735"],["dc.identifier.isi","000293282700068"],["dc.identifier.pmid","21818378"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8201"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22616"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Targeted Ablation of Oligodendrocytes Triggers Axonal Damage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","354"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Host & Microbe"],["dc.bibliographiccitation.lastpage","365.e5"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Remy, Melissa M."],["dc.contributor.author","Sahin, Mehmet"],["dc.contributor.author","Flatz, Lukas"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Xu, Lifen"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Fallet, Benedict"],["dc.contributor.author","Doras, Camille"],["dc.contributor.author","Rieger, Toni"],["dc.contributor.author","Bestmann, Lukas"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Kaufmann, Beat A."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.date.accessioned","2020-12-10T14:23:06Z"],["dc.date.available","2020-12-10T14:23:06Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.chom.2017.07.008"],["dc.identifier.issn","1931-3128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71834"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interferon-γ-Driven iNOS: A Molecular Pathway to Terminal Shock in Arenavirus Hemorrhagic Fever"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","984"],["dc.bibliographiccitation.issue","6071"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","989"],["dc.bibliographiccitation.volume","335"],["dc.contributor.author","Bonilla, Weldy V."],["dc.contributor.author","Froehlich, Anja"],["dc.contributor.author","Senn, Karin"],["dc.contributor.author","Kallert, Sandra"],["dc.contributor.author","Fernandez, Marylise"],["dc.contributor.author","Johnson, Susan"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Hegazy, Ahmed N."],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Fallon, Padraic G."],["dc.contributor.author","Klemenz, Roman"],["dc.contributor.author","Nakae, Susumu"],["dc.contributor.author","Adler, Heiko"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Loehning, Max"],["dc.contributor.author","Pinschewer, Daniel D."],["dc.date.accessioned","2018-11-07T09:13:18Z"],["dc.date.available","2018-11-07T09:13:18Z"],["dc.date.issued","2012"],["dc.description.abstract","Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as damage-associated molecular patterns or alarmins, remains ill defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8(+) T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a CTL-intrinsic fashion, determined plurifunctional effector cell differentiation, and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses."],["dc.identifier.doi","10.1126/science.1215418"],["dc.identifier.isi","000300931800051"],["dc.identifier.pmid","22323740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27144"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Advancement Science"],["dc.relation.issn","0036-8075"],["dc.title","The Alarmin Interleukin-33 Drives Protective Antiviral CD8(+) T Cell Responses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","367"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Jafari, Mehrnoosh"],["dc.contributor.author","Schumacher, Adrian-Minh"],["dc.contributor.author","Snaidero, Nicolas"],["dc.contributor.author","Ullrich Gavilanes, Emily M."],["dc.contributor.author","Neziraj, Tradite"],["dc.contributor.author","Kocsis-Jutka, Virág"],["dc.contributor.author","Engels, Daniel"],["dc.contributor.author","Jürgens, Tanja"],["dc.contributor.author","Wagner, Ingrid"],["dc.contributor.author","Weidinger, Juan Daniel Flórez"],["dc.contributor.author","Schmidt, Stephanie S."],["dc.contributor.author","Beltrán, Eduardo"],["dc.contributor.author","Hagan, Nellwyn"],["dc.contributor.author","Woodworth, Lisa"],["dc.contributor.author","Ofengeim, Dimitry"],["dc.contributor.author","Gans, Joseph"],["dc.contributor.author","Wolf, Fred"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Portugues, Ruben"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2021-04-14T08:30:17Z"],["dc.date.available","2021-04-14T08:30:17Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41593-020-00780-7"],["dc.identifier.pmid","33495636"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83177"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/12"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/103"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B03: Checkpoints of recovery after primary astrocytic lesions in neuromyelitis optica and related animal models"],["dc.relation","TRR 274 | C02: In vivo detection and targeting of calcium clearance and axonal membrane repair after acute CNS insults"],["dc.relation","TRR 274 | C05: Checkpoints for circuit integration of nascent neurons in the injured brain"],["dc.relation","TRR 274 | Z01: Bioimaging Platform"],["dc.relation","TRR 274 | Z02: Genomics and Bioinformatics Platform"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | C02: Aktive Zonendesigns und -dynamiken, die auf das synaptische Arbeitsgedächtnis zugeschnitten sind"],["dc.relation.eissn","1546-1726"],["dc.relation.issn","1097-6256"],["dc.relation.workinggroup","RG Kerschensteiner (Neuroimmune Interactions)"],["dc.relation.workinggroup","RG Misgeld"],["dc.relation.workinggroup","RG Portugues (Sensorimotor Control)"],["dc.relation.workinggroup","RG Wolf"],["dc.title","Phagocyte-mediated synapse removal in cortical neuroinflammation is promoted by local calcium accumulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","231"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","246"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Rodriguez, Enrique Garea"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Neid, Katharina"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Juergens, Tanja"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Merkler, Doron"],["dc.date.accessioned","2018-11-07T09:37:11Z"],["dc.date.available","2018-11-07T09:37:11Z"],["dc.date.issued","2014"],["dc.description.abstract","Cerebral cortex shows a high endogenous propensity for remyelination. Yet, widespread subpial cortical demyelination (SCD) is a common feature in progressive multiple sclerosis (MS) and can already be found in early MS. In the present study, we compared oligodendroglial loss in SCD in early and chronic MS. Furthermore, we addressed in an experimental model whether repeated episodes of inflammatory SCD could alter oligodendroglial repopulation and subsequently lead to persistently demyelinated cortical lesions. NogoA(+) mature oligodendrocytes and Olig2(+) oligodendrocyte precursor cells were examined in SCD in patients with early and chronic MS, normal-appearing MS cortex, and control cortex as well as in the rat model of repeated targeted cortical experimental autoimmune encephalomyelitis (EAE). NogoA(+) and Olig2(+) cells were significantly reduced in SCD in patients with chronic, but not early MS. Repeated induction of SCD in rats resulted only in a transient loss of NogoA(+), but not Olig2(+) cells during the demyelination phase. This phase was followed by complete oligodendroglial repopulation and remyelination, even after four episodes of demyelination. Our data indicate efficient oligodendroglial repopulation in subpial cortical lesions in rats after repeated SCD that was similar to early, but not chronic MS cases. Accordingly, four cycles of experimental de- and remyelination were not sufficient to induce sustained remyelination failure as found in chronic cortical MS lesions. This suggests that alternative mechanisms contribute to oligodendrocyte depletion in chronic cortical demyelination in MS."],["dc.identifier.doi","10.1007/s00401-014-1260-8"],["dc.identifier.isi","000339725800005"],["dc.identifier.pmid","24563023"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32782"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Oligodendroglia in cortical multiple sclerosis lesions decrease with disease progression, but regenerate after repeated experimental demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]