Winkler, Anne

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Haberl, Michael"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Gao, Ming"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Thal, Dietmar R."],["dc.contributor.author","Chang, Mayland"],["dc.contributor.author","Opdenakker, Ghislain"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2021-04-14T08:28:11Z"],["dc.date.available","2021-04-14T08:28:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1172/JCI141694"],["dc.identifier.pmid","33645550"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82526"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/22"],["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 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Odoardi (Echtzeitdarstellung neuroimmunologischer Prozesse)"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.title","Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","523"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","538"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Kayser, Dieter M."],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:42:12Z"],["dc.date.available","2018-11-07T09:42:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuromyelitis optica (NMO) is a chronic, mostly relapsing inflammatory demyelinating disease of the CNS characterized by serum anti-aquaporin 4 (AQP4) antibodies in the majority of patients. Anti-AQP4 antibodies derived from NMO patients target and deplete astrocytes in experimental models when co-injected with complement. However, the time course and mechanisms of oligodendrocyte loss and demyelination and the fate of oligodendrocyte precursor cells (OPC) have not been examined in detail. Also, no studies regarding astrocyte repopulation of experimental NMO lesions have been reported. We utilized two rat models using either systemic transfer or focal intracerebral injection of recombinant human anti-AQP4 antibodies to generate NMO-like lesions. Time-course experiments were performed to examine oligodendroglial and astroglial damage and repair. In addition, oligodendrocyte pathology was studied in early human NMO lesions. Apart from early complement-mediated astrocyte destruction, we observed a prominent, very early loss of oligodendrocytes and oligodendrocyte precursor cells (OPCs) as well as a delayed loss of myelin. Astrocyte repopulation of focal NMO lesions was already substantial after 1 week. Olig2-positive OPCs reappeared before NogoA-positive, mature oligodendrocytes. Thus, using two experimental models that closely mimic the human disease, our study demonstrates that oligodendrocyte and OPC loss is an extremely early feature in the formation of human and experimental NMO lesions and leads to subsequent, delayed demyelination, highlighting an important difference in the pathogenesis of MS and NMO."],["dc.identifier.doi","10.1007/s00401-013-1220-8"],["dc.identifier.isi","000332957400005"],["dc.identifier.pmid","24292009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33902"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Early loss of oligodendrocytes in human and experimental neuromyelitis optica lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","314"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","322"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Enz, Lukas"],["dc.contributor.author","Goebels, Norbert"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T10:11:38Z"],["dc.date.available","2018-11-07T10:11:38Z"],["dc.date.issued","2016"],["dc.description.abstract","Breakdown of myelin sheaths is a pathological hallmark of several autoimmune diseases of the nervous system. We employed autoantibody-mediated animal models of demyelinating diseases, including a rat model of neuromyelitis optica (NMO), to target myelin and found that myelin lamellae are broken down into vesicular structures at the innermost region of the myelin sheath. We demonstrated that myelin basic proteins (MBP), which form a polymer in between the myelin membrane layers, are targeted in these models. Elevation of intracellular Ca2+ levels resulted in MBP network disassembly and myelin vesiculation. We propose that the aberrant phase transition of MBP molecules from their cohesive to soluble and non-adhesive state is a mechanism triggering myelin breakdown in NMO and possibly in other demyelinating diseases."],["dc.identifier.doi","10.1016/j.celrep.2016.06.008"],["dc.identifier.isi","000380262300005"],["dc.identifier.pmid","27346352"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13675"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40088"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Loss of Myelin Basic Protein Function Triggers Myelin Breakdown in Models of Demyelinating Diseases"],["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","34"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","35"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:33:34Z"],["dc.date.available","2018-11-07T09:33:34Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.094"],["dc.identifier.isi","000345192100087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31993"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Early breakdown of the blood-brain barrier in a model of neuromyelitis optica"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Brain"],["dc.contributor.author","Herwerth, Marina"],["dc.contributor.author","Kenet, Selin"],["dc.contributor.author","Schifferer, Martina"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Weber, Melanie"],["dc.contributor.author","Snaidero, Nicolas"],["dc.contributor.author","Wang, Mengzhe"],["dc.contributor.author","Lohrberg, Melanie"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Misgeld, Thomas"],["dc.date.accessioned","2022-04-01T10:02:49Z"],["dc.date.available","2022-04-01T10:02:49Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Neuromyelitis optica (NMO) is a chronic neuroinflammatory disease, which primarily targets astrocytes and often results in severe axon injury of unknown mechanism. NMO patients harbor autoantibodies against the astrocytic water channel protein, aquaporin-4 (AQP4-IgG), which induce complement-mediated astrocyte lysis and subsequent axon damage. Using spinal in vivo imaging in a mouse model of such astrocytopathic lesions, we explored the mechanism underlying NMO-related axon injury. Many axons showed a swift and morphologically distinct ‘pearls-on-string’ transformation also readily detectable in human NMO lesions, which especially affected small caliber axons independently of myelination. Functional imaging revealed that calcium homeostasis was initially preserved in this ‘acute axonal beading’ state, ruling out disruption of the axonal membrane, which sets this form of axon injury apart from previously described forms of traumatic and inflammatory axon damage. Morphological, pharmacological and genetic analyses showed that AQP4-IgG-induced axon injury involved osmotic stress and ionic overload, but does not appear to use canonical pathways of Wallerian-like degeneration. Subcellular analysis of beaded axons demonstrated remodeling of the axonal cytoskeleton in beaded axons, especially local loss of microtubules. Treatment with the microtubule stabilizer epothilone, a therapy in development for traumatic and degenerative axonopathies, prevented axonal beading, while destabilizing microtubules sensitized axons for beading. Our results reveal a distinct form of immune-mediated axon pathology in NMO that mechanistically differs from known cascades of posttraumatic and inflammatory axon loss, and suggest a new strategy for neuroprotection in NMO and related diseases."],["dc.identifier.doi","10.1093/brain/awac079"],["dc.identifier.pmid","35202467"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106013"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/454"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/59"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Misgeld"],["dc.relation.workinggroup","RG Schifferer"],["dc.rights","CC BY-NC 4.0"],["dc.title","A new form of axonal pathology in a spinal model of neuromyelitis optica"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]