Schultz, Verena

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T09:33:35Z"],["dc.date.available","2018-11-07T09:33:35Z"],["dc.date.issued","2014"],["dc.format.extent","129"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.346"],["dc.identifier.isi","000345192100336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31999"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Axonal damage and protection during early remyelination in multiple sclerosis and an animal model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","246"],["dc.contributor.author","Lescher, Juliane"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Redenbach, Laura"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Here we demonstrate that miRNA regulation in marmoset (Callithrix jacchus) and C57/BL6 mouse EAE lesions largely resembles miRNA regulation in active human MS lesions. Detailed quantitative PCR analyses of the most up- and downregulated miRNAs of active human MS lesions in dissected lesions from marmoset EAE brains and inflamed spinal cords of EAE mice revealed that the conserved and highly regulated miRNAs, miRNA-155, miRNA-142-3p, miRNA-146a, miRNA-146b and miRNA-21, turned out to be similarly upregulated in marmoset and mouse EAE lesions. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2012.02.012"],["dc.identifier.gro","3142535"],["dc.identifier.isi","000304026900004"],["dc.identifier.pmid","22445295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8897"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","MicroRNA regulation in experimental autoimmune encephalomyelitis in mice and marmosets resembles regulation in human multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Cumberworth, Stephanie L."],["dc.contributor.author","Barrie, Jennifer A."],["dc.contributor.author","Cunningham, Madeleine E."],["dc.contributor.author","de Figueiredo, Daniely Paulino Gomes"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Wilder-Smith, Adrian J."],["dc.contributor.author","Brennan, Benjamin"],["dc.contributor.author","Pena, Lindomar J."],["dc.contributor.author","Freitas de Oliveira França, Rafael"],["dc.contributor.author","Edgar, Julia M."],["dc.date.accessioned","2021-06-01T10:48:07Z"],["dc.date.available","2021-06-01T10:48:07Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1186/s40478-017-0450-8"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85832"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2051-5960"],["dc.title","Zika virus tropism and interactions in myelinating neural cell cultures: CNS cells and myelin are preferentially affected"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","eaam7816"],["dc.bibliographiccitation.issue","419"],["dc.bibliographiccitation.journal","Science Translational Medicine"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Fard, Maryam K."],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Sánchez, Paula"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Mandad, Sunit"],["dc.contributor.author","Jäkel, Sarah"],["dc.contributor.author","Fornasiero, Eugenio F."],["dc.contributor.author","Schmitt, Sebastian"],["dc.contributor.author","Ehrlich, Marc"],["dc.contributor.author","Starost, Laura"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Sergiou, Christina"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Dimou, Leda"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2020-12-10T18:36:46Z"],["dc.date.available","2020-12-10T18:36:46Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1126/scitranslmed.aam7816"],["dc.identifier.eissn","1946-6242"],["dc.identifier.issn","1946-6234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76735"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","BCAS1 expression defines a population of early myelinating oligodendrocytes in multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","202"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","203"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, A."],["dc.date.accessioned","2018-11-07T10:08:48Z"],["dc.date.available","2018-11-07T10:08:48Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Biogen; Novartis; Genzyme; Teva"],["dc.identifier.isi","000383267201212"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39538"],["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","pH and K-V channel conductance are not central to damage of demyelinated axons in the cuprizone mouse model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","860410"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Crawford, Colin L."],["dc.contributor.author","Antoniou, Christina"],["dc.contributor.author","Komarek, Lina"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Donald, Claire L."],["dc.contributor.author","Montague, Paul"],["dc.contributor.author","Barnett, Susan C."],["dc.contributor.author","Linington, Christopher"],["dc.contributor.author","Willison, Hugh J."],["dc.contributor.author","Kohl, Alain"],["dc.contributor.author","Edgar, Julia M."],["dc.date.accessioned","2022-06-01T09:39:53Z"],["dc.date.available","2022-06-01T09:39:53Z"],["dc.date.issued","2022"],["dc.description.abstract","Zika virus (ZIKV) is a neurotropic flavivirus recently linked to congenital ZIKV syndrome in children and encephalitis and Guillain-Barré syndrome in adults. Neurotropic viruses often use axons to traffic to neuronal or glial cell somas where they either remain latent or replicate and proceed to infect new cells. Consequently, it has been suggested that axon degeneration could represent an evolutionarily conserved mechanism to limit viral spread. Whilst it is not known if ZIKV transits in axons, we previously reported that ZIKV infection of glial cells in a murine spinal cord-derived cell culture model of the CNS is associated with a profound loss of neuronal cell processes. This, despite that postmitotic neurons are relatively refractory to infection and death. Here, we tested the hypothesis that ZIKV-associated degeneration of neuronal processes is dependent on activation of Sterile alpha and armadillo motif-containing protein 1 (SARM1), an NADase that acts as a central executioner in a conserved axon degeneration pathway. To test this, we infected wild type and Sarm1 homozygous or heterozygous null cell cultures with ZIKV and examined NAD + levels as well as the survival of neurons and their processes. Unexpectedly, ZIKV infection led to a rapid SARM1-independent reduction in NAD + . Nonetheless, the subsequent profound loss of neuronal cell processes was SARM1-dependent and was preceded by early changes in the appearance of β-tubulin III staining. Together, these data identify a role for SARM1 in the pathogenesis of ZIKV infection, which may reflect SARM1's conserved prodegenerative function, independent of its NADase activity."],["dc.description.sponsorship"," Horizon 2020"],["dc.description.sponsorship"," Medical Research Council"],["dc.description.sponsorship"," Chief Scientist Office, Scottish Government Health and Social Care Directorate"],["dc.description.sponsorship"," Gates Cambridge Trust"],["dc.description.sponsorship"," John and Lucille Van Geest Foundation"],["dc.identifier.doi","10.3389/fnmol.2022.860410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108586"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1662-5099"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","SARM1 Depletion Slows Axon Degeneration in a CNS Model of Neurotropic Viral Infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1350"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1360"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T10:21:54Z"],["dc.date.available","2018-11-07T10:21:54Z"],["dc.date.issued","2017"],["dc.description.abstract","Remyelination is in the center of new therapies for the treatment of multiple sclerosis to resolve and improve disease symptoms and protect axons from further damage. Although remyelination is considered beneficial in the long term, it is not known, whether this is also the case early in lesion formation. Additionally, the precise timing of acute axonal damage and remyelination has not been assessed so far. To shed light onto the interrelation between axons and the myelin sheath during de-and remyelination, we employed cuprizone- and focal lysolecithin-induced demyelination and performed time course experiments assessing the evolution of early and late stage remyelination and axonal damage. We observed damaged axons with signs of remyelination after cuprizone diet cessation and lysolecithin injection. Similar observations were made in early multiple sclerosis lesions. To assess the correlation of remyelination and axonal damage in multiple sclerosis lesions, we took advantage of a cohort of patients with early and late stage remyelinated lesions and assessed the number of APP- and SMI32- positive damaged axons and the density of SMI31- positive and silver impregnated preserved axons. Early de-and remyelinating lesions did not differ with respect to axonal density and axonal damage, but we observed a lower axonal density in late stage demyelinated multiple sclerosis lesions than in remyelinated multiple sclerosis lesions. Our findings suggest that remyelination may not only be protective over a long period of time, but may play an important role in the immediate axonal recuperation after a demyelinating insult."],["dc.identifier.doi","10.1002/glia.23167"],["dc.identifier.isi","000403348100009"],["dc.identifier.pmid","28560740"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Acutely damaged axons are remyelinated in multiple sclerosis and experimental models of demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]