Stadelmann-Nessler, Christine

[["dc.bibliographiccitation.firstpage","923"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","936"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Schwabenland, Marius"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Prinz, Marco"],["dc.date.accessioned","2021-12-01T09:23:07Z"],["dc.date.available","2021-12-01T09:23:07Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract As extremely sensitive immune cells, microglia act as versatile watchdogs of the central nervous system (CNS) that tightly control tissue homeostasis. Therefore, microglial activation is an early and easily detectable hallmark of virtually all neuropsychiatric, neuro-oncological, neurodevelopmental, neurodegenerative and neuroinflammatory diseases. The recent introduction of novel high-throughput technologies and several single-cell methodologies as well as advances in epigenetic analyses helped to identify new microglia expression profiles, enhancer-landscapes and local signaling cues that defined diverse previously unappreciated microglia states in the healthy and diseased CNS. Here, we give an overview on the recent developments in the field of microglia biology and provide a practical guide to analyze disease-associated microglia phenotypes in both the murine and human CNS, on several morphological and molecular levels. Finally, technical limitations, potential pitfalls and data misinterpretations are discussed as well."],["dc.description.abstract","Abstract As extremely sensitive immune cells, microglia act as versatile watchdogs of the central nervous system (CNS) that tightly control tissue homeostasis. Therefore, microglial activation is an early and easily detectable hallmark of virtually all neuropsychiatric, neuro-oncological, neurodevelopmental, neurodegenerative and neuroinflammatory diseases. The recent introduction of novel high-throughput technologies and several single-cell methodologies as well as advances in epigenetic analyses helped to identify new microglia expression profiles, enhancer-landscapes and local signaling cues that defined diverse previously unappreciated microglia states in the healthy and diseased CNS. Here, we give an overview on the recent developments in the field of microglia biology and provide a practical guide to analyze disease-associated microglia phenotypes in both the murine and human CNS, on several morphological and molecular levels. Finally, technical limitations, potential pitfalls and data misinterpretations are discussed as well."],["dc.identifier.doi","10.1007/s00401-021-02370-8"],["dc.identifier.pii","2370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94564"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Analyzing microglial phenotypes across neuropathologies: a practical guide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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.firstpage","793"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","796"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Lucchinetti, C."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T08:59:26Z"],["dc.date.available","2018-11-07T08:59:26Z"],["dc.date.issued","2001"],["dc.description.abstract","Severe tissue destruction is the presumed histopathological correlate of hypointense multiple sclerosis (MS) lesions. In this study we correlated changes of lesion hypointensity over time with initial histopathological features in 14 biopsied MS lesions. The extent of hypointensity increased in initially demyelinated plaques and decreased in remyelinating lesions. The initial axonal loss determined the increase of hypointensity over time. In conclusion, both axonal loss and demyelinating activity determine the evolution of hypointensity over time."],["dc.identifier.doi","10.1002/ana.1053"],["dc.identifier.isi","000169091400016"],["dc.identifier.pmid","11409432"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23896"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","A longitudinal MRI study of histopathologically defined hypointense 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","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.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:35:31Z"],["dc.date.available","2018-11-07T10:35:31Z"],["dc.date.issued","2003"],["dc.format.extent","389"],["dc.identifier.isi","000185600700017"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45118"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","48th Annual Meeting of the German-Society-for-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Permanent axonal loss in EAE in WLDs mice occurs independently of Wallerian degeneration"],["dc.type","conference_abstract"],["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.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","181"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","185"],["dc.bibliographiccitation.volume","206"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2022-03-01T11:45:28Z"],["dc.date.available","2022-03-01T11:45:28Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S0022-510X(02)00191-0"],["dc.identifier.pii","S0022510X02001910"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103341"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0022-510X"],["dc.title","Remyelination in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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"]]