König, Fatima Barbara

[["dc.bibliographiccitation.firstpage","7"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","16"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Achenboch, S."],["dc.contributor.author","Berger, T."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Konig, F."],["dc.contributor.author","Morales, Y."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Bryants, S."],["dc.contributor.author","Moore, S. B."],["dc.contributor.author","Keegan, B. M."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T11:07:09Z"],["dc.date.available","2018-11-07T11:07:09Z"],["dc.date.issued","2007"],["dc.description.abstract","Controversy exists regarding the pathogenic or predictive role of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with multiple sclerosis (MS). Four immunopathological patterns (IP) have been recognized in early active MS lesions, suggesting heterogeneous pathogenic mechanisms. Whether MOG antibodies contribute to this pathological heterogeneity and potentially serve as biomarkers to identify specific pathological patterns is unknown. Here we report the frequencies of antibodies to human recombinant MOG (identified by Western blot and enzyme-linked immunoabsorbent assay (ELISA)) in patients with pathologically proven demyelinating disease, and investigate whether antibody status is associated with clinical course, HLA-DR2-genotype, IP or treatment response to plasmapheresis. The biopsy cohort consisted of 72 patients: 12 pattern 1, 43 pattern 11 and 17 pattern Ill. No association was found between MOG antibody status and conversion to clinically definite MS, DR-2 status, IP or response to plasmapheresis. There was poor agreement between Western blot and ELISA (kappa = 0.07 for MOG IgM). Fluctuations in antibody seropositivity were seen for 3/4 patients tested serially by Western blot. This study does not support a pathologic pattern-specific role for MOG-antibodies. Variable MOG-antibody status on serial measurements, coupled with the lack of Western blot and ELISA correlations, raises concern regarding the use of MOG-antibody as an MS biomarker and underscores the need for methodological consensus."],["dc.description.sponsorship","NCRR NIH HHS [M01 RR00585]"],["dc.identifier.doi","10.1177/1352458506072189"],["dc.identifier.isi","000243823800001"],["dc.identifier.pmid","17294606"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12982"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52483"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1352-4585"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Myelin oligodendrocyte glycoprotein antibodies in pathologically proven multiple sclerosis: frequency, stability and clinicopathologic correlations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7032"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kantarci, O. H."],["dc.contributor.author","Ziemer, P."],["dc.contributor.author","Konig, F."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:46:07Z"],["dc.date.available","2018-11-07T10:46:07Z"],["dc.date.issued","2004"],["dc.format.extent","S154"],["dc.identifier.isi","000225459800202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47671"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Arnold, Hodder Headline Plc"],["dc.publisher.place","London"],["dc.relation.conference","20th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple- Sclerosis/9th Annual Meeting of Rehabilitation in MS"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","1352-4585"],["dc.title","Gender differences in immunopathological patterns of multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1693"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","1697"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","McClelland, R. L."],["dc.contributor.author","Achenbach, S. J."],["dc.contributor.author","Konig, F."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Scheithauer, Bernd W."],["dc.contributor.author","Rodriguez, M."],["dc.contributor.author","Weinshenker, Brian G."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:53:55Z"],["dc.date.available","2018-11-07T10:53:55Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: A pathological classification has been developed of early active multiple sclerosis ( MS) lesions that reveals four patterns of tissue injury: I - T cell/macrophage associated; II - antibody/ complement associated; III - distal oligodendrogliopathy, and IV - oligodendrocyte degeneration in the periplaque white matter. Mechanisms of demyelination in early MS may differ among the subgroups. Previous studies on biopsied MS have lacked clinicopathological correlation and follow up. Critics argue that observations are not generalisable to prototypic MS. Objective: To describe the clinicopathological characteristics of the MS Lesion Project biopsy cohort. Methods: Clinical characteristics and disability of patients with pathologically confirmed inflammatory demyelinating disease ( excluding ADEM) classified immunopathologically ( n = 91) and patients from the Olmsted County MS prevalence cohort ( n = 218) were determined. Results: Most patients who underwent biopsy and had pathologically proved demyelinating disease ultimately developed definite ( n = 70) or probable ( n = 12) MS ( median follow up 4.4 years). Most had a relapsing remitting course and 73% were ambulatory (EDSS <= 4) at last follow up. Nine patients remained classified as having an isolated demyelinating syndrome at last follow up. Patients with different immunopathological patterns had similar clinical characteristics. Although presenting symptoms and sex ratios differed, the clinical course in biopsy patients was similar to the prevalence cohort. Median EDSS was <4.0 in both cohorts when matched for disease duration, sex, and age. Conclusions: Most patients undergoing biopsy, who had pathologically confirmed demyelinating disease, were likely to develop MS and remain ambulatory after a median disease duration of 4.4 years. The immunopathological patterns lacked specific clinical correlations and were not related to the timing of the biopsy. These data suggest that pathogenic implications derived largely from MS biopsy studies may be extrapolated to the general MS population."],["dc.description.sponsorship","NCRR NIH HHS [M01 RR00585]"],["dc.identifier.doi","10.1136/jnnp.2004.060624"],["dc.identifier.isi","000233316900018"],["dc.identifier.pmid","16291895"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49454"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","B M J Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Clinical course, pathological correlations, and outcome of biopsy proved inflammatory demyelinating disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]