Wegner, Christiane

[["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","John, Gareth R."],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Nisimov, Liat Hayardeny"],["dc.contributor.author","Piryatinsky, Victor"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:11:32Z"],["dc.date.available","2018-11-07T09:11:32Z"],["dc.date.issued","2012"],["dc.identifier.isi","000303204802032"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26743"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","64th Annual Meeting of the American-Academy-of-Neurology (AAN)"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0028-3878"],["dc.title","Laquinimod Protects from Cuprizone-Induced Demyelination through Modulation of Astrocyte Activation Via Interfering with the NF kappa-B Pathway"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1762"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1764"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Goertz, Chantima"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Berlit, Peter"],["dc.date.accessioned","2018-11-07T08:38:38Z"],["dc.date.available","2018-11-07T08:38:38Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1007/s00415-010-5611-7"],["dc.identifier.isi","000282700300032"],["dc.identifier.pmid","20559846"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18807"],["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","Primary angiitis of the CNS with pure spinal cord involvement: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["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","229"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Opinion in Neurology"],["dc.bibliographiccitation.lastpage","234"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Albert, Monika"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2021-06-01T10:46:54Z"],["dc.date.available","2021-06-01T10:46:54Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose of review Multiple sclerosis is the most common chronic, disabling central nervous system disease in young adults, characterized by inflammatory demyelinating white matter lesions with glial scar formation and axonal loss. Lately, evidence has accumulated that large areas of grey matter are affected in multiple sclerosis patients. Recent findings Findings in post-mortem brain tissue support the notion that cortical demyelination is frequent and extensive, especially in patients with chronic multiple sclerosis. Cortical lesions differ from white matter lesions with respect to inflammatory cell infiltration, gliosis, and remyelination. Thus, differences in cortical and white matter lesion pathogenesis have been proposed. Experimental models suggest a decisive role for antimyelin antibodies in cortical demyelination. Topical studies focus on damage to neurons, dendrites, and synapses in cortical multiple sclerosis lesions. Improved imaging techniques for the detection of cortical lesions are currently developed and will provide the basis for future clinicopathological correlative studies. Summary In summary, recent years have opened our eyes to the extensive grey matter involvement in multiple sclerosis. Studies on the pathogenesis of cortical demyelination, cortical damage, and repair will elucidate basic principles of multiple sclerosis lesion formation. However, more sensitive imaging tools are required to study the impact of cortical lesions on clinical symptoms, disability, and disease progression."],["dc.identifier.doi","10.1097/01.wco.0000318863.65635.9a"],["dc.identifier.isi","000256183400002"],["dc.identifier.pmid","18451703"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85418"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1350-7540"],["dc.title","Cortical pathology 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","411"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","424"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Pham, Trinh"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Piryatinsky, Victor"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Brakelmann, Lars"],["dc.contributor.author","Hagemeier, Karin"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","John, Gareth R."],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:06:50Z"],["dc.date.available","2018-11-07T09:06:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Laquinimod (LAQ) is a new oral immunomodulatory compound that reduces relapse rate, brain atrophy and disability progression in multiple sclerosis (MS). LAQ has well-documented effects on inflammation in the periphery, but little is known about its direct activity within the central nervous system (CNS). To elucidate the impact of LAQ on CNS-intrinsic inflammation, we investigated the effects of LAQ on cuprizone-induced demyelination in mice in vivo and on primary CNS cells in vitro. Demyelination, inflammation, axonal damage and glial pathology were evaluated in LAQ-treated wild type and Rag-1-deficient mice after cuprizone challenge. Using primary cells we tested for effects of LAQ on oligodendroglial survival as well as on cytokine secretion and NF-kappa B activation in astrocytes and microglia. LAQ prevented cuprizone-induced demyelination, microglial activation, axonal transections, reactive gliosis and oligodendroglial apoptoses in wild type and Rag-1-deficient mice. LAQ significantly decreased pro-inflammatory factors in stimulated astrocytes, but not in microglia. Oligodendroglial survival was not affected by LAQ in vitro. Astrocytic, but not microglial, NF-kappa B activation was markedly reduced by LAQ as evidenced by NF-kappa B reporter assay. LAQ also significantly decreased astrocytic NF-kappa B activation in cuprizone-treated mice. Our data indicate that LAQ prevents cuprizone-induced demyelination by attenuating astrocytic NF-kappa B activation. These effects are CNS-intrinsic and not mediated by peripheral immune cells. Therefore, LAQ downregulation of the astrocytic pro-inflammatory response may be an important mechanism underlying its protective effects on myelin, oligodendrocytes and axons. Modulation of astrocyte activation may be an attractive therapeutic target to prevent tissue damage in MS."],["dc.identifier.doi","10.1007/s00401-012-1009-1"],["dc.identifier.isi","000307757200010"],["dc.identifier.pmid","22766690"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25641"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Reduced astrocytic NF-kappa B activation by laquinimod protects from cuprizone-induced 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"]]

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","464"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Helms, Gunther"],["dc.contributor.author","Garea-Rodriguez, Enrique"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T10:12:06Z"],["dc.date.available","2018-11-07T10:12:06Z"],["dc.date.issued","2016"],["dc.description.abstract","Multiple sclerosis (MS) is the most common cause for sustained disability in young adults, yet treatment options remain very limited. Although numerous therapeutic approaches have been effective in rodent models of experimental autoimmune encephalomyelitis (EAE), only few proved to be beneficial in patients with MS. Hence, there is a strong need for more predictive animal models. Within the past decade, EAE in the common marmoset evolved as a potent, alternative model for MS, with immunological and pathological features resembling more closely the human disease. However, an often very rapid and severe disease course hampers its implementation for systematic testing of new treatment strategies. We here developed a new focal model of EAE in the common marmoset, induced by myelin oligodendrocyte glycoprotein (MOG) immunization and stereotactic injections of proinflammatory cytokines. At the injection site of cytokines, confluent inflammatory demyelinating lesions developed that strongly resembled human MS lesions. In a proof-of-principle treatment study with the immunomodulatory compound laquinimod, we demonstrate that targeted EAE in marmosets provides a promising and valid tool for preclinical experimental treatment trials in MS research."],["dc.identifier.doi","10.1111/bpa.12292"],["dc.identifier.isi","000380034000002"],["dc.identifier.pmid","26207848"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40173"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.title","A New Targeted Model of Experimental Autoimmune Encephalomyelitis in the Common Marmoset"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:02:17Z"],["dc.date.available","2018-11-07T09:02:17Z"],["dc.date.issued","2012"],["dc.format.extent","172"],["dc.identifier.isi","000312764800462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","11th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","0165-5728"],["dc.title","Laquinimod reduces astrocytic NF kappa B activation in vitro and 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","756"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","766"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:54:01Z"],["dc.date.available","2018-11-07T09:54:01Z"],["dc.date.issued","2015"],["dc.description.abstract","Remyelination capacity decreases with age in adult mice, but data comparing remyelination capacity after toxic demyelination in developing mice versus adult mice are not available. We treated 3-week-old and adult C57BL/6 mice with cuprizone for 1 to 5 weeks and studied demyelination/remyelination and cellular reactions in the corpus callosum and motor cortex by histology, immunohistochemistry, and electron microscopy. We compared results between the 2 treated groups and age-matched controls. In juvenile mice, significant demyelination was detectable in the corpus callosum on Week 2 and in the motor cortex on Week 5. Oligodendrocyte loss, microglial activation, and acute axonal damage peaked on Week 2. Increased numbers of oligodendrocyte precursor cells were evident on Week 1, and remyelination was detectable on Week 3. Juvenile mice showed more rapid demyelination than adult mice, which may be related to greater vulnerability of oligodendrocytes, lower myelin content, or dose-dependent cuprizone effects. Earlier activation of microglia and proliferation of oligodendrocyte precursor cells probably contributed to accelerated remyelination and less pronounced axonal damage. Our data indicate that oligodendroglial regeneration and remyelination are enhanced in the maturing rodent brain compared with the young-adult rodent brain."],["dc.identifier.doi","10.1097/NEN.0000000000000214"],["dc.identifier.isi","000358657300001"],["dc.identifier.pmid","26115190"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36452"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Remyelination After Cuprizone-Induced Demyelination Is Accelerated in Juvenile Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1308"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1319"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Menken, Lena"],["dc.contributor.author","Pförtner, Ramona"],["dc.contributor.author","Schmid, Susanne N."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2020-12-10T14:06:33Z"],["dc.date.available","2020-12-10T14:06:33Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/glia.23605"],["dc.identifier.issn","0894-1491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69943"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.issn","0894-1491"],["dc.title","Glial fibrillary acidic protein expression alters astrocytic chemokine release and protects mice from cuprizone-induced demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","275"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease"],["dc.bibliographiccitation.lastpage","282"],["dc.bibliographiccitation.volume","1812"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:59:44Z"],["dc.date.available","2018-11-07T08:59:44Z"],["dc.date.issued","2011"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system which responds to anti-inflammatory treatments in the early disease phase. However, the pathogenesis of the progressive disease phase is less well understood, and inflammatory as well as neurodegenerative mechanisms of tissue damage are currently being discussed. This review summarizes current knowledge on the interrelation between inflammation, demyelination, and neurodegeneration derived from the study of human autopsy and biopsy brain tissue and experimental models of MS. (C) 2010 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbadis.2010.07.007"],["dc.identifier.isi","000286681500017"],["dc.identifier.pmid","20637864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23974"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0925-4439"],["dc.title","Inflammation, demyelination, and degeneration - Recent insights from MS pathology"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]