Brück, Wolfgang

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Jentoft, Mark E."],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Lennon, Vanda A."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Weinshenker, Brian G."],["dc.contributor.author","Wingerchuk, Dean M."],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Shuster, Elizabeth A."],["dc.contributor.author","Carter, Jonathan"],["dc.contributor.author","Boyd, Clara D."],["dc.contributor.author","Clardy, Stacey Lynn"],["dc.contributor.author","Cohen, Bruce A."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:02:13Z"],["dc.date.available","2018-11-07T10:02:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: To assess, in a surgical biopsy cohort of active demyelinating lesions, the diagnostic utility of aquaporin-4 (AQP4) immunohistochemistry in identifying neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD) and describe pathologic features that should prompt AQP4 immunohistochemical analysis and AQP4-immunoglobulin G (IgG) serologic testing. Methods: This was a neuropathologic cohort study of 20 surgical biopsies (19 patients; 11 cord/9 brain), performed because of diagnostic uncertainty, interpreted as active demyelinating disease and containing 2 or more of the following additional features: tissue vacuolation, granulocytic infiltrates, or astrocyte injury. Results: AQP4 immunoreactivity was lost in 18 biopsies and increased in 2. Immunopathologic features of the AQP4 loss cohort were myelin vacuolation (18), dystrophic astrocytes and granulocytes (17), vascular hyalinization (16), macrophages containing glial fibrillary acid protein (GFAP)-positive debris (14), and Creutzfeldt-Peters cells (0). All 14 cases with available serum tested positive for AQP4-IgG after biopsy. Diagnosis at last follow-up was NMO/NMOSD (15) and longitudinally extensive transverse myelitis (1 each relapsing and single). Immunopathologic features of the AQP4 increased cohort were macrophages containing GFAP-positive debris and granulocytes (2), myelin vacuolation (1), dystrophic astrocytes (1), Creutzfeldt-Peters cells (1), and vascular hyalinization (1). Diagnosis at last follow-up was multiple sclerosis (MS) and both tested AQP4-IgG seronegative after biopsy. Conclusions: AQP4 immunohistochemistry with subsequent AQP4-IgG testing has diagnostic utility in identifying cases of NMO/NMOSD. This study highlights the importance of considering NMOSD in the differential diagnosis of tumefactive brain or spinal cord lesions. AQP4-IgG testing may avert biopsy and avoid ineffective therapies if these patients are erroneously treated for MS."],["dc.identifier.isi","000347996400012"],["dc.identifier.pmid","25503621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Diagnostic utility of aquaporin-4 in the analysis of active demyelinating lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1906"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e1913"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Tobin, W. Oliver"],["dc.contributor.author","Kalinowska-Lyszczarz, Alicja"],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Tosakulwong, Nirubol"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2021-12-01T09:22:30Z"],["dc.date.available","2021-12-01T09:22:30Z"],["dc.date.issued","2021"],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.identifier.doi","10.1212/WNL.0000000000012782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94416"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Clinical Correlation of Multiple Sclerosis Immunopathologic Subtypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","235"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Radue, Ernst-Wilhelm"],["dc.contributor.author","Oterino, Agustin"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Kuhle, Jens"],["dc.contributor.author","Sahraian, Mohammad Ali"],["dc.contributor.author","Gray, Francoise"],["dc.contributor.author","Jakl, Veronika"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:13:35Z"],["dc.date.available","2018-11-07T09:13:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Natalizumab is an approved medication for highly active multiple sclerosis (MS). Progressive multifocal leukoencephalopathy (PML) may occur as a severe side effect of this drug. Here, we describe pathological and radiological characteristics of immune reconstitution inflammatory syndrome (IRIS), which occurs in natalizumab-associated PML after the cessation of therapy, and we differentiate it from ongoing PML. Brain biopsy tissue and MRI scans from five MS patients with natalizumab-associated PML were analyzed and their histology compared with non-MS PML. Histology showed an extensive CD8-dominated T cell infiltrate and numerous macrophages within lesions, and in nondemyelinated white and grey matter, in four out of five cases. Few or no virally infected cells were found. This was indicative of IRIS as known from HIV patients with PML. Outstandingly high numbers of plasma cells were present as compared to non-MS PML and typical MS lesions. MRI was compatible with IRIS, revealing enlarging lesions with a band-like or speckled contrast enhancement either at the lesion edge or within lesions. Only the fifth patient showed typical PML pathology, with low inflammation and high numbers of virally infected cells. This patient showed a similar interval between drug withdrawal and biopsy (3.5 months) to the rest of the cohort (range 2.5-4 months). MRI could not differentiate between PML-associated IRIS and ongoing PML. We describe in detail the histopathology of IRIS in natalizumab-associated PML. PML-IRIS, ongoing PML infection, and MS exacerbation may be impossible to discern clinically alone. MRI may provide some clues for distinguishing different pathologies that can be differentiated histologically. In our individual cases, biopsy helped to clarify diagnoses in natalizumab-associated PML."],["dc.identifier.doi","10.1007/s00401-011-0900-5"],["dc.identifier.isi","000301855900007"],["dc.identifier.pmid","22057786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27215"],["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","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Pathology of immune reconstitution inflammatory syndrome in multiple sclerosis with natalizumab-associated progressive multifocal leukoencephalopathy"],["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.artnumber","81"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Rieckmann, Peter"],["dc.contributor.author","Kallmann, Boris-Alexander"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2019-07-09T11:42:51Z"],["dc.date.available","2019-07-09T11:42:51Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1186/s40478-016-0352-1"],["dc.identifier.pmid","27503238"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58763"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Disseminated necrotizing leukoencephalopathy eight months after alemtuzumab treatment for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13275"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Romanelli, Elisa"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Mezydlo, Aleksandra"],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Nikic, Ivana"],["dc.contributor.author","Potz, Stephanie"],["dc.contributor.author","Meinl, Edgar"],["dc.contributor.author","Matznick, Florian E. H."],["dc.contributor.author","Kreutzfeldt, Mario"],["dc.contributor.author","Ghanem, Alexander"],["dc.contributor.author","Conzelmann, Karl-Klaus"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Routh, Matthew"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Bishop, Derron"],["dc.contributor.author","Misgeld, Thomas"],["dc.contributor.author","Kerschensteiner, Martin"],["dc.date.accessioned","2018-11-07T10:05:43Z"],["dc.date.available","2018-11-07T10:05:43Z"],["dc.date.issued","2016"],["dc.description.abstract","Oligodendrocyte damage is a central event in the pathogenesis of the common neuro-inflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge."],["dc.identifier.doi","10.1038/ncomms13275"],["dc.identifier.isi","000387837900001"],["dc.identifier.pmid","27848954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38953"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model"],["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.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Lucchinetti, C."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2018-11-07T10:08:49Z"],["dc.date.available","2018-11-07T10:08:49Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Biogen; Novartis; Genzyme"],["dc.format.extent","367"],["dc.identifier.isi","000383267201480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39540"],["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","Apheresis therapy in multiple sclerosis patients with histopathologically classified immunopathological patterns"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1618"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","1632"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","von Gottberg, Phillip"],["dc.contributor.author","Pulkowski, Ulrich"],["dc.contributor.author","Kirsten, Florian"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Rauer, Sebastian"],["dc.contributor.author","Scheibe, Franziska"],["dc.contributor.author","Radbruch, Helena"],["dc.contributor.author","Hammer, Eckhard"],["dc.contributor.author","Stürner, Klarissa H"],["dc.contributor.author","Kaulen, Barbara"],["dc.contributor.author","Heesen, Christoph"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Brock, Sebastian"],["dc.contributor.author","Pawlitzki, Marc"],["dc.contributor.author","Bopp, Tobias"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2020-12-10T18:38:31Z"],["dc.date.available","2020-12-10T18:38:31Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1177/1352458518819098"],["dc.identifier.eissn","1477-0970"],["dc.identifier.issn","1352-4585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77350"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Severe meningo-/encephalitis after daclizumab therapy for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e33"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology® neuroimmunology & neuroinflammation"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Thomas, Katja"],["dc.contributor.author","Dietze, Kristin"],["dc.contributor.author","Wehner, Rebekka"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Schultheiß, Thorsten"],["dc.contributor.author","Günther, Claudia"],["dc.contributor.author","Schäkel, Knut"],["dc.contributor.author","Reichmann, Heinz"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Schmitz, Marc"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.date.accessioned","2015-10-20T13:57:53Z"],["dc.date.accessioned","2021-10-27T13:20:20Z"],["dc.date.available","2015-10-20T13:57:53Z"],["dc.date.available","2021-10-27T13:20:20Z"],["dc.date.issued","2014-10-01"],["dc.description.abstract","OBJECTIVE: To examine the potential role of 6-sulfo LacNAc(+) (slan) dendritic cells (DCs) displaying pronounced proinflammatory properties in the pathogenesis of multiple sclerosis (MS). METHODS: We determined the presence of slanDCs in demyelinated brain lesions and CSF samples of patients with MS. In addition, we explored the impact of methylprednisolone, interferon-β, glatiramer acetate, or natalizumab on the frequency of blood-circulating slanDCs in patients with MS. We also evaluated whether interferon-β modulates important proinflammatory capabilities of slanDCs. RESULTS: SlanDCs accumulate in highly inflammatory brain lesions and are present in the majority of CSF samples of patients with MS. Short-term methylprednisolone administration reduces the percentage of slanDCs in blood of patients with MS and the proportion of tumor necrosis factor-α- or CD150-expressing slanDCs. Long-term interferon-β treatment decreases the percentage of blood-circulating slanDCs in contrast to glatiramer acetate or natalizumab. Furthermore, interferon-β inhibits the secretion of proinflammatory cytokines by slanDCs and their capacity to promote proliferation and differentiation of T cells. CONCLUSION: Accumulation of slanDCs in highly inflammatory brain lesions and their presence in CSF indicate that slanDCs may play an important role in the immunopathogenesis of MS. The reduction of blood-circulating slanDCs and the inhibition of their proinflammatory properties by methylprednisolone and interferon-β may contribute to the therapeutic efficiency of these drugs in patients with MS."],["dc.identifier.doi","10.1212/NXI.0000000000000033"],["dc.identifier.fs","611429"],["dc.identifier.pmid","25340085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91957"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2332-7812"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Accumulation and therapeutic modulation of 6-sulfo LacNAc(+) dendritic cells in multiple sclerosis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S131"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","S132"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Zeis, Thomas"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.date.accessioned","2018-11-07T11:23:42Z"],["dc.date.available","2018-11-07T11:23:42Z"],["dc.date.issued","2009"],["dc.identifier.isi","000270075500546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56245"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","Hoboken"],["dc.relation.conference","9th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","0894-1491"],["dc.title","GENE EXPRESSION ANALYSIS OF PARAFFIN EMBEDDED BIOPSIES FROM EARLY MS CASES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","91"],["dc.bibliographiccitation.volume","286"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Goldschmidt, Thomas"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Wegner, C."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:22:05Z"],["dc.date.available","2018-11-07T11:22:05Z"],["dc.date.issued","2009"],["dc.description.abstract","Multiple sclerosis (MS) lesions are histopathologically characterized by inflammation, demyelination/remyelination, axonal damage and gliosis. Animal experimental and in vitro studies suggest that sex hormones influence the immune system and contribute to the increased likelihood in women of developing MS. However, a variety of studies have also shown that remyelination is more marked in female rodents or that female sex hormones are beneficial for myelin repair. To determine whether gender influences the histopathology of MS lesions, we compared the extent of inflammation, axonal damage and remyelination in MS lesions of female and male MS patients. We observed no differences in the composition of inflammatory infiltrates, axonal damage or cortical pathology. Similar numbers of oligodendroglial progenitor cells and mature oligodendrocytes were present in MS lesions. Remyelination is slightly, but not significantly, more extensive in women than men in early MS lesions. The absence of significant differences in lesion pathology between female and male MS patients might be explained by a lack of a gender influence, but also might be due to the limited number of tissue samples available for histopathological analysis. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2009.07.014"],["dc.identifier.isi","000271621800020"],["dc.identifier.pmid","19674757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55923"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","14th European-Charcot-Foundation Symposium"],["dc.relation.eventlocation","Taormina, ITALY"],["dc.relation.issn","0022-510X"],["dc.title","Gender differences in the histopathology of MS?"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]