Pfeifenbring, Sabine

[["dc.bibliographiccitation.firstpage","807"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","815"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Haider, Lukas"],["dc.contributor.author","Zrzavy, Tobias"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Hoeftberger, Romana"],["dc.contributor.author","Bagnato, Francesca"],["dc.contributor.author","Grabner, Guenther"],["dc.contributor.author","Trattnig, Siegfried"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T10:17:40Z"],["dc.date.available","2018-11-07T10:17:40Z"],["dc.date.issued","2016"],["dc.description.abstract","Multiple sclerosis is characterized by widespread primary demyelination and progressive degeneration, driven by heterogeneous mechanisms. Haider et al. provide a topographic map of the frequency with which different brain regions are affected by these processes, and show that demyelination and neurodegeneration involve inflammatory as well as vascular changes.Multiple sclerosis is characterized by widespread primary demyelination and progressive degeneration, driven by heterogeneous mechanisms. Haider et al. provide a topographic map of the frequency with which different brain regions are affected by these processes, and show that demyelination and neurodegeneration involve inflammatory as well as vascular changes.Multiple sclerosis is a chronic inflammatory disease with primary demyelination and neurodegeneration in the central nervous system. In our study we analysed demyelination and neurodegeneration in a large series of multiple sclerosis brains and provide a map that displays the frequency of different brain areas to be affected by these processes. Demyelination in the cerebral cortex was related to inflammatory infiltrates in the meninges, which was pronounced in invaginations of the brain surface (sulci) and possibly promoted by low flow of the cerebrospinal fluid in these areas. Focal demyelinated lesions in the white matter occurred at sites with high venous density and additionally accumulated in watershed areas of low arterial blood supply. Two different patterns of neurodegeneration in the cortex were identified: oxidative injury of cortical neurons and retrograde neurodegeneration due to axonal injury in the white matter. While oxidative injury was related to the inflammatory process in the meninges and pronounced in actively demyelinating cortical lesions, retrograde degeneration was mainly related to demyelinated lesions and axonal loss in the white matter. Our data show that accumulation of lesions and neurodegeneration in the multiple sclerosis brain does not affect all brain regions equally and provides the pathological basis for the selection of brain areas for monitoring regional injury and atrophy development in future magnetic resonance imaging studies."],["dc.identifier.doi","10.1093/brain/awv398"],["dc.identifier.isi","000371694600023"],["dc.identifier.pmid","26912645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41276"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","The topograpy of demyelination and neurodegeneration in the multiple sclerosis brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Wimmer, Isabella"],["dc.contributor.author","Haider, L."],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T09:18:49Z"],["dc.date.available","2018-11-07T09:18:49Z"],["dc.date.issued","2013"],["dc.format.extent","9"],["dc.identifier.isi","000328751400004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28488"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","29th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis / 18th Annual Conference of Rehabilitation in MS"],["dc.relation.eventlocation","Copenhagen, DENMARK"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Iron and oxidative damage in the multiple sclerosis brain"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","848"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","861"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Wimmer, Isabella"],["dc.contributor.author","Haider, Lukas"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T09:16:47Z"],["dc.date.available","2018-11-07T09:16:47Z"],["dc.date.issued","2013"],["dc.description.abstract","ObjectiveIron may contribute to the pathogenesis and progression of multiple sclerosis (MS) due to its accumulation in the human brain with age. Our study focused on nonheme iron distribution and the expression of the iron-related proteins ferritin, hephaestin, and ceruloplasmin in relation to oxidative damage in the brain tissue of 33 MS and 30 control cases. MethodsWe performed (1) whole-genome microarrays including 4 MS and 3 control cases to analyze the expression of iron-related genes, (2) nonheme iron histochemistry, (3) immunohistochemistry for proteins of iron metabolism, and (4) quantitative analysis by digital densitometry and cell counting in regions representing different stages of lesion maturation. ResultsWe found an age-related increase of iron in the white matter of controls as well as in patients with short disease duration. In chronic MS, however, there was a significant decrease of iron in the normal-appearing white matter (NAWM) corresponding with disease duration, when corrected for age. This decrease of iron in oligodendrocytes and myelin was associated with an upregulation of iron-exporting ferroxidases. In active MS lesions, iron was apparently released from dying oligodendrocytes, resulting in extracellular accumulation of iron and uptake into microglia and macrophages. Iron-containing microglia showed signs of cell degeneration. At lesion edges and within centers of lesions, iron accumulated in astrocytes and axons. InterpretationIron decreases in the NAWM of MS patients with increasing disease duration. Cellular degeneration in MS lesions leads to waves of iron liberation, which may propagate neurodegeneration together with inflammatory oxidative burst. Ann Neurol 2013;74:848-861"],["dc.description.sponsorship","Austrian Science Fund [P24245-B19]"],["dc.identifier.doi","10.1002/ana.23974"],["dc.identifier.isi","000329891100015"],["dc.identifier.pmid","23868451"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28011"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Iron and Neurodegeneration in the Multiple Sclerosis Brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","12"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Bunyan, Reem F."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:05:35Z"],["dc.date.available","2018-11-07T09:05:35Z"],["dc.date.issued","2012"],["dc.identifier.isi","000328702200008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25356"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Lyon, FRANCE"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Axonal damage in inflammatory demyelinating lesions of paediatric patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Bunyan, Reem F."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Gaertner, J."],["dc.contributor.author","Lucchinetti, Claudia F."],["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.format.extent","67"],["dc.identifier.isi","000383267200107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39527"],["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","Oligodendroglial damage and remyelination in paediatric multiple sclerosis lesions."],["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","655"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","667"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Bunyan, Reem F."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Roever, Christian"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2017-09-07T11:44:29Z"],["dc.date.available","2017-09-07T11:44:29Z"],["dc.date.issued","2015"],["dc.description.abstract","ObjectiveAxonal damage occurs early in multiple sclerosis (MS) and contributes to the degree of clinical disability. Children with MS more often show disabling and polyfocal neurological symptoms at disease onset than adults with MS. Thus, axonal damage may differ between pediatric and adult MS patients. MethodsWe analyzed axonal pathology in archival brain biopsy and autopsy samples from 19 children with early MS. Lesions were classified according to demyelinating activity and presence of remyelination. Axonal density and extent of acute axonal damage were assessed using Bielschowsky silver impregnation and immunohistochemistry for amyloid precursor protein (APP), respectively. Axonal injury was correlated with the inflammatory infiltrate as well as clinical characteristics. Results were compared with data from adult MS patients. ResultsAcute axonal damage was most extensive in early active demyelinating (EA) lesions of pediatric patients and correlated positively with the Expanded Disability Status Scale at attack leading to biopsy/autopsy. Comparison with 12 adult patients showed a 50% increase in the extent of acute axonal damage in EA lesions from children compared to adults, with the highest number of APP-positive spheroids found prior to puberty. The extent of acute axonal damage correlated positively with the number of lesional macrophages. Axonal density was reduced in pediatric lesions irrespective of the demyelinating activity or the presence of remyelination. Axonal reduction was similar between children and adults. InterpretationOur results provide evidence for more pronounced acute axonal damage in inflammatory demyelinating lesions from children compared to adults. Ann Neurol 2015;77:655-667"],["dc.identifier.doi","10.1002/ana.24364"],["dc.identifier.gro","3141935"],["dc.identifier.isi","000352102500010"],["dc.identifier.pmid","25612167"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2713"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley-blackwell"],["dc.relation.eissn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Extensive Acute Axonal Damage in Pediatric 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.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:51:29Z"],["dc.date.available","2018-11-07T08:51:29Z"],["dc.date.issued","2011"],["dc.format.extent","S143"],["dc.identifier.isi","000209137300285"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21944"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","P57kiP2 is not dynamically regulated in remyelinating multiple sclerosis lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","382"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Multiple Sclerosis"],["dc.bibliographiccitation.lastpage","387"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Hummel, Hannah-Maria"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stark, Wiebke"],["dc.contributor.author","Huppke, Brenda"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Because of the emergence of novel therapies for multiple sclerosis (MS) and the associated increased risk of progressive multifocal leukoencephalopathy, John Cunningham (JC) virus infection has become a focus of interest for neurologists. However, little is known about JC virus infection in pediatric MS to date. Objective: We aimed to analyze the prevalence of anti-JC virus antibodies, the conversion rate and the influence of the anti-JC virus antibody status on the clinical course in a large pediatric MS cohort. Methods: Anti-JC virus antibodies were analyzed in serum samples within six months of disease onset and during the course of the disease. Clinical data were extracted from a pediatric MS databank. Results: A total of 51.6% of 256 patients were found to be positive for anti-JC virus antibodies at onset of disease. No correlation between antibody status and clinical course was seen. Analyzing 693 follow-up serum samples revealed high titer stability, and an annual conversion rate of 4.37% was seen. Conclusion: No evidence was found that seropositivity for anti-JC virus antibodies influences the clinical course. Surprisingly, seroprevalence for anti-JC virus antibodies was more than twice as high as anticipated in this age group, raising the question of whether the infection increases the risk of MS development."],["dc.identifier.doi","10.1177/1352458514543340"],["dc.identifier.gro","3141931"],["dc.identifier.isi","000352165000006"],["dc.identifier.pmid","25070674"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2668"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","JC virus antibody status in a pediatric multiple sclerosis cohort: Prevalence, conversion rate and influence on disease severity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","658"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuropathology and Applied Neurobiology"],["dc.bibliographiccitation.lastpage","661"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","von Baumgarten, L."],["dc.contributor.author","Schueller, Ulrich"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Wirtz, C. R."],["dc.contributor.author","Hecht, Marie-Lyn"],["dc.contributor.author","Terpolilli, N. A."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:37:23Z"],["dc.date.available","2018-11-07T09:37:23Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1111/nan.12089"],["dc.identifier.isi","000339003200014"],["dc.identifier.pmid","24117509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32829"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1365-2990"],["dc.relation.issn","0305-1846"],["dc.title","Biopsy findings of symptomatic cerebral X-linked adrenoleucodystrophy and histological differentiation from multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]