Wegner, Christiane

[["dc.bibliographiccitation.firstpage","399"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Current Neurology and Neuroscience Reports"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T11:24:39Z"],["dc.date.available","2018-11-07T11:24:39Z"],["dc.date.issued","2009"],["dc.description.abstract","Gray matter demyelination is frequent and extensive in most patients with multiple sclerosis (MS) and has recently received much attention in neuropathologic and imaging studies. Gray matter lesions show distinct pathologic features that make their detection difficult with conventional imaging techniques. Thus, despite their high prevalence, their impact on clinical symptoms has not been defined well so far. This review focuses on recent information from pathologic and imaging studies and summarizes our current knowledge on cortical pathology derived from human and experimental studies."],["dc.identifier.doi","10.1007/s11910-009-0058-x"],["dc.identifier.isi","000268572700008"],["dc.identifier.pmid","19664370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56452"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1528-4042"],["dc.title","Gray matter pathology and multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","471"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical & Experimental Metastasis"],["dc.bibliographiccitation.lastpage","482"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Stadelmann, Chr."],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:26:31Z"],["dc.date.available","2018-11-07T09:26:31Z"],["dc.date.issued","2013"],["dc.description.abstract","An essential function of the transcription factors LEF1/TCF4 in cerebral metastases of lung adenocarcinomas has been described in mouse models, suggesting a WNT/beta-catenin effect as potential mechanism. Their role in humans is still unclear, thus we analyzed LEF1, TCF4, beta-catenin, and early stage prognostic markers in 25 adenocarcinoma brain metastases using immunohistochemistry (IHC). IHC revealed nuclear TCF4 in all adenocarcinoma samples, whereas only 36 % depicted nuclear LEF1 and nuclear beta-catenin signals. Samples with nuclear LEF1 as well as high TCF4 (++++) expression were associated with a shorter survival (p = 0.01, HR = 6.68), while nuclear beta-catenin had no significant impact on prognosis and did not significantly correlate with nuclear LEF1. High proliferation index Ki67 was associated with shorter survival in late-stage disease (p = 0.03, HR 3.27). Additionally, we generated a LEF1/TCF4 as well as an AXIN2 signature, the latter as representative of WNT/beta-catenin activity, following a bioinformatics approach with a gene expression dataset of cerebral metastases in lung adenocarcinoma. To analyze the prognostic relevance in primary lung adenocarcinomas, we applied both signatures to a microarray dataset of 58 primary lung adenocarcinomas. Only the LEF1/TCF4 signature was able to separate clusters with impact on survival (p = 0.01, HR = 0.32). These clusters displayed diverging enrichment patterns of the cell cycle pathway. In conclusion, our data show that LEF1/TCF4, but not beta-catenin, have prognostic relevance in primary and cerebrally metastasized human lung adenocarcinomas. In contrast to the previous in vivo findings, these results indicate that LEF1/TCF4 act independently of beta-catenin in this setting."],["dc.identifier.doi","10.1007/s10585-012-9552-7"],["dc.identifier.isi","000317297400011"],["dc.identifier.pmid","23224985"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30319"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1573-7276"],["dc.relation.issn","0262-0898"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Nuclear LEF1/TCF4 correlate with poor prognosis but not with nuclear beta-catenin in cerebral metastasis of lung adenocarcinomas"],["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","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","85"],["dc.bibliographiccitation.journal","Neuroscience & Biobehavioral Reviews"],["dc.bibliographiccitation.lastpage","98"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Parmar, Katrin"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Rocca, Maria A."],["dc.contributor.author","Langdon, Dawn"],["dc.contributor.author","D'Angelo, Egidio"],["dc.contributor.author","D’Souza, Marcus"],["dc.contributor.author","Burggraaff, Jessica"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Sastre-Garriga, Jaume"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Dorn, Jonas"],["dc.contributor.author","Uitdehaag, Bernard M.J."],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Wuerfel, Jens"],["dc.contributor.author","Enzinger, Christian"],["dc.contributor.author","Rovira, Alex"],["dc.contributor.author","Tintore, Mar"],["dc.contributor.author","Filippi, Massimo"],["dc.contributor.author","Kappos, Ludwig"],["dc.contributor.author","Sprenger, Till"],["dc.date.accessioned","2020-12-10T15:20:25Z"],["dc.date.available","2020-12-10T15:20:25Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.neubiorev.2018.02.012"],["dc.identifier.issn","0149-7634"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72663"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The role of the cerebellum in multiple sclerosis—150 years after Charcot"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]