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Metz, Imke
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Metz, Imke
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Metz, Imke
Alternative Name
Metz, I.
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2017Journal Article [["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","64"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Webb, Samuel M."],["dc.contributor.author","Tham, Mylyne"],["dc.contributor.author","Adiele, Reginald C."],["dc.contributor.author","Robinson, Christopher A."],["dc.contributor.author","Fitz-Gibbon, Patrick D."],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Nehzati, Susan"],["dc.contributor.author","George, Graham N."],["dc.contributor.author","Pickering, Ingrid J."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Yong, Guo"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) in which oligodendrocytes, the CNS cells that stain most robustly for iron and myelin are the targets of injury. Metals are essential for normal CNS functioning, and metal imbalances have been linked to demyelination and neuro-degeneration. Using a multidisciplinary approach involving synchrotron techniques, iron histochemistry and immunohistochemistry, we compared the distribution and quantification of iron and zinc in MS lesions to the surrounding normal appearing and periplaque white matter, and assessed the involvement of these metals in MS lesion pathogenesis. We found that the distribution of iron and zinc is heterogeneous in MS plaques, and with few remarkable exceptions they do not accumulate in chronic MS lesions. We show that brain iron tends to decrease with increasing age and disease duration of MS patients; reactive astrocytes organized in large astrogliotic areas in a subset of smoldering and inactive plaques accumulate iron and safely store it in ferritin; a subset of smoldering lesions do not contain a rim of iron-loaded macrophages/microglia; and the iron content of shadow plaques varies with the stage of remyelination. Zinc in MS lesions was generally decreased, paralleling myelin loss. Iron accumulates concentrically in a subset of chronic inactive lesions suggesting that not all iron rims around MS lesions equate with smoldering plaques. Upon degeneration of iron-loaded microglia/macrophages, astrocytes may form an additional protective barrier that may prevent iron-induced oxidative damage."],["dc.identifier.doi","10.1007/s00401-017-1696-8"],["dc.identifier.isi","000403235900004"],["dc.identifier.pmid","28332093"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14717"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42219"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Pathogenic implications of distinct patterns of iron and zinc in chronic MS lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2021Journal Article Research Paper [["dc.bibliographiccitation.journal","Brain Pathology"],["dc.contributor.author","Häusler, Darius"],["dc.contributor.author","Akgün, Katja"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2021-06-01T09:42:00Z"],["dc.date.available","2021-06-01T09:42:00Z"],["dc.date.issued","2021"],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.1111/bpa.12969"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85110"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1750-3639"],["dc.relation.issn","1015-6305"],["dc.relation.orgunit","Institut für Neuropathologie"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","CNS inflammation after natalizumab therapy for multiple sclerosis: A retrospective histopathological and CSF cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2015Journal Article [["dc.bibliographiccitation.firstpage","263"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","277"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Licht-Mayer, Simon"],["dc.contributor.author","Wimmer, Isabella"],["dc.contributor.author","Traffehn, Sarah"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Bauer, Jan"],["dc.contributor.author","Bradl, Monika"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T09:54:06Z"],["dc.date.available","2018-11-07T09:54:06Z"],["dc.date.issued","2015"],["dc.description.abstract","Oxidative injury appears to play a major role in the propagation of demyelination and neurodegeneration in multiple sclerosis (MS). It has been suggested that endogenous anti-oxidant defense mechanisms within MS lesions are insufficient to prevent spreading of damage. Thus, current therapeutic approaches (e.g., fumarate treatment) target to up-regulate the expression of a key regulator of anti-oxidative defense, the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). In this study, we show that Nrf2 is already strongly up-regulated in active MS lesions. Nuclear Nrf2 expression was particularly observed in oligodendrocytes and its functional activity is indicated by the expression of one of its downstream targets (heme oxygenase 1) in the same cells. In contrast, only a minor number of Nrf2-positive neurons were detected, even in highly inflammatory cortical lesions presenting with extensive oxidative injury. Overall, the most pronounced Nrf2 expression was found in degenerating cells, which showed signs of apoptotic or necrotic cell death. Via whole-genome microarray analyses of MS lesions, we observed a differential expression of numerous Nrf2-responsive genes, also involved in the defense against oxidative stress, predominantly in areas of initial myelin destruction within actively demyelinating white matter lesions. Furthermore, the expression patterns of Nrf2-induced genes differed between the white matter and cortical gray matter. Our study shows that in the MS brain, Nrf2 expression varies in different cell types and is associated with active demyelination in the lesions."],["dc.identifier.doi","10.1007/s00401-015-1452-x"],["dc.identifier.isi","000358025300008"],["dc.identifier.pmid","26087903"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11966"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36469"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cell type-specific Nrf2 expression in multiple sclerosis lesions"],["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"]]Details DOI PMID PMC WOS