Nessler, Stefan

[["dc.bibliographiccitation.firstpage","1590"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1593"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:39:53Z"],["dc.date.available","2018-11-07T08:39:53Z"],["dc.date.issued","2010"],["dc.description.abstract","The following review summarizes the progress in multiple sclerosis research published in the Journal of Neurology in 2009."],["dc.identifier.doi","10.1007/s00415-010-5689-y"],["dc.identifier.isi","000281250100031"],["dc.identifier.pmid","20689961"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5157"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19106"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Advances in multiple sclerosis research in 2009"],["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","19057"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","19062"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Zhou, D."],["dc.contributor.author","Srivastava, Rajneesh"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Grummel, Verena"],["dc.contributor.author","Sommer, Norbert"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T08:51:00Z"],["dc.date.available","2018-11-07T08:51:00Z"],["dc.date.issued","2006"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Although the cause of MS is still uncertain, many findings point toward an ongoing autoimmune response to myelin antigens. Because of its location on the outer surface of the myelin sheath and its pathogenicity in the experimental autoimmune encephalomyelitis model, myelin oligodendrocyte glycoprotein (MOG) is one of the potential disease-causing self antigens in MS. However, the role of MOG in the pathogenesis of MS has remained controversial. In this study we addressed the occurrence of autoantibodies to native MOG and its implication for demyelination and axonal loss in MS. We applied a high-sensitivity bioassay, which allowed detecting autoantibodies that bind to the extracellular part of native MOG. Antibodies, mostly IgG, were found in sera that bound with high affinity to strictly conformational epitopes of the extracellular domain of MOG. IgG but not IgM antibody titers to native MOG were significantly higher in MS patients compared with different control groups with the highest prevalence in primary progressive MS patients. Serum autoantibodies to native MOG induced death of MOG-expressing target cells in vitro. Serum from MS patients with high anti-MOG antibody titers stained white matter myelin in rat brain and enhanced demyelination and axonal damage when transferred to autoimmune encephalomyelitis animals. Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients."],["dc.identifier.doi","10.1073/pnas.0607242103"],["dc.identifier.isi","000242884200034"],["dc.identifier.pmid","17142321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in 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","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bittner, Alwina"],["dc.contributor.author","Schlegel, Kerstin"],["dc.contributor.author","Gronen, Felix"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Sommer, Norbert"],["dc.date.accessioned","2018-11-07T09:11:30Z"],["dc.date.available","2018-11-07T09:11:30Z"],["dc.date.issued","2006"],["dc.description.abstract","Substance P (SP) is an excitatory neurotransmitter in the central and peripheral nervous system. Most of its physiological functions are mediated through binding to the neurokinin-1 receptor (NK-1R). Recently, proinflammatory properties of SP have been described. In this study we utilized T cell transfer experimental autoimmune encephalomyelitis (EAE) to investigate the role of SP in CNS autoimmune disease. Treatment with the NK-1R antagonist CP-96,345 dramatically reduced clinical and histological signs of EAE if administered before disease onset. The protective effect of CP96,345 treatment was related to a reduced expression of the adhesion molecules ICAM-1 and VCAM-1 on CNS endothelia. The cellular composition or activation status of splenocytes was not affected by CP-96,345 administration, while the secretion of proinflammatory Thl cytokines was reduced in treated animals. Th2 cytokines remained largely unaffected by NK-1 receptor antagonist treatment. In summary, our findings suggest that the protective effect of CP96,345 treatment is mediated by stabilization of the blood-brain barrier and suppression of Thl immunity. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.06.026"],["dc.identifier.isi","000241821800001"],["dc.identifier.pmid","16904192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26735"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Suppression of autoimmune encephalomyelitis by a neurokinin-1 receptor antagonist - A putative role for substance P in CNS inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.firstpage","79"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Avendano-Guzman, E."],["dc.contributor.author","Theiss, R."],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T10:08:45Z"],["dc.date.available","2018-11-07T10:08:45Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Teva; Biogen; Novartis; Genzyme"],["dc.identifier.isi","000383267200129"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","A new rodent model of progressive demyelination and neurodegeneration mimicking progressive MS."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T08:51:35Z"],["dc.date.available","2018-11-07T08:51:35Z"],["dc.date.issued","2011"],["dc.format.extent","S154"],["dc.identifier.isi","000294178900605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21968"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.issn","0894-1491"],["dc.title","TISSUE DAMAGE AND REPAIR AFTER SELECTIVE ASTROCYTE DEPLETION IN VIVO"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","814"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuropathology and Applied Neurobiology"],["dc.bibliographiccitation.lastpage","831"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2018-11-07T09:50:34Z"],["dc.date.available","2018-11-07T09:50:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Aims: Natalizumab is a humanized monoclonal antibody specific for CD49d receptors of integrins. It inhibits the entry of inflammatory cells into the central nervous system and is approved for the treatment of relapsing-remitting multiple sclerosis (MS). Several lines of evidence indicate an involvement of B cells and plasma cells in MS pathogenesis. However, treatment with the natalizumab analogon PS/2 immunoglobulin G (IgG) has so far only been investigated in T cell-mediated animal models of MS. Due to the importance of B lineage cells in the pathogenesis of MS, the objective of the present study has thus been to analyse the effects of PS/2 IgG in a mouse model of MS with T and B cell cooperation (OSE mice). Methods: OSE mice were treated with the natalizumab analogon PS/2 IgG either at disease onset or after peak of disease. Treatment was also performed with PS/2 F(ab')2 fragments. Results: PS/2 IgG treatment improved the clinical outcome and decreased spinal cord demyelination and immune cell infiltration if given early in the disease course. Treatment increased blood leukocytes and resulted in a partial internalization of CD49d in T and B cells. The therapeutic effects of PS/2 IgG injections were independent of the Fc fragment as F(ab') 2 injections were equally beneficial. In contrast, PS/2 IgG was not effective when given late in the disease course. Conclusions: Results indicate that natalizumab may also be beneficial in MS with B cell-driven immunopathogenesis."],["dc.description.sponsorship","DFG Transregional Collaborative Research Group [TRR-SFB 43]"],["dc.identifier.doi","10.1111/nan.12220"],["dc.identifier.isi","000364640500008"],["dc.identifier.pmid","25641089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35732"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1365-2990"],["dc.relation.issn","0305-1846"],["dc.title","Natalizumab analogon therapy is effective in a B cell-dependent multiple sclerosis model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T09:05:36Z"],["dc.date.available","2018-11-07T09:05:36Z"],["dc.date.issued","2012"],["dc.format.extent","127"],["dc.identifier.isi","000328702200244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25360"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Lyon, FRANCE"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Protection of oligodendroglia in experimental NMO lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","448"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","449"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Wegner, C."],["dc.contributor.author","Ott, M."],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Lund, B. T."],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:18:52Z"],["dc.date.available","2018-11-07T09:18:52Z"],["dc.date.issued","2013"],["dc.identifier.isi","000328751403036"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28501"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","29th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis / 18th Annual Conference of Rehabilitation in MS"],["dc.relation.eventlocation","Copenhagen, DENMARK"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Laquinimod induces a shift in natural killer cell populations in mice with experimental autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]