Linker, Ralf Andreas

[["dc.bibliographiccitation.firstpage","678"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","692"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Ryan, Sarah"],["dc.contributor.author","van Dam, Anne M."],["dc.contributor.author","Conrad, Rebecca"],["dc.contributor.author","Bista, Pradeep"],["dc.contributor.author","Zeng, Weike"],["dc.contributor.author","Hronowsky, Xiaoping"],["dc.contributor.author","Buko, Alex"],["dc.contributor.author","Chollate, Sowmya"],["dc.contributor.author","Ellrichmann, Gisa"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Dawson, Kate"],["dc.contributor.author","Goelz, Susan"],["dc.contributor.author","Wiese, Stefan"],["dc.contributor.author","Scannevin, Robert H."],["dc.contributor.author","Lukashev, Matvey"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T08:59:01Z"],["dc.date.available","2018-11-07T08:59:01Z"],["dc.date.issued","2011"],["dc.description.abstract","Inflammation and oxidative stress are thought to promote tissue damage in multiple sclerosis. Thus, novel therapeutics enhancing cellular resistance to free radicals could prove useful for multiple sclerosis treatment. BG00012 is an oral formulation of dimethylfumarate. In a phase II multiple sclerosis trial, BG00012 demonstrated beneficial effects on relapse rate and magnetic resonance imaging markers indicative of inflammation as well as axonal destruction. First we have studied effects of dimethylfumarate on the disease course, central nervous system, tissue integrity and the molecular mechanism of action in an animal model of chronic multiple sclerosis: myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis in C57BL/6 mice. In the chronic phase of experimental autoimmune encephalomyelitis, preventive or therapeutic application of dimethylfumarate ameliorated the disease course and improved preservation of myelin, axons and neurons. In vitro, the application of fumarates increased murine neuronal survival and protected human or rodent astrocytes against oxidative stress. Application of dimethylfumarate led to stabilization of the transcription factor nuclear factor (erythroid-derived 2)-related factor 2, activation of nuclear factor (erythroid-derived 2)-related factor 2-dependent transcriptional activity and accumulation of NADP(H) quinoline oxidoreductase-1 as a prototypical target gene. Furthermore, the immediate metabolite of dimethylfumarate, monomethylfumarate, leads to direct modification of the inhibitor of nuclear factor (erythroid-derived 2)-related factor 2, Kelch-like ECH-associated protein 1, at cysteine residue 151. In turn, increased levels of nuclear factor (erythroid-derived 2)-related factor 2 and reduced protein nitrosylation were detected in the central nervous sytem of dimethylfumarate-treated mice. Nuclear factor (erythroid-derived 2)-related factor 2 was also upregulated in the spinal cord of autopsy specimens from untreated patients with multiple sclerosis. In dimethylfumarate-treated mice suffering from experimental autoimmune encephalomyelitis, increased immunoreactivity for nuclear factor (erythroid-derived 2)-related factor 2 was detected by confocal microscopy in neurons of the motor cortex and the brainstem as well as in oligodendrocytes and astrocytes. In mice deficient for nuclear factor (erythroid-derived 2)-related factor 2 on the same genetic background, the dimethylfumarate mediated beneficial effects on clinical course, axon preservation and astrocyte activation were almost completely abolished thus proving the functional relevance of this transcription factor for the neuroprotective mechanism of action. We conclude that the ability of dimethylfumarate to activate nuclear factor (erythroid-derived 2)-related factor 2 may offer a novel cytoprotective modality that further augments the natural antioxidant responses in multiple sclerosis tissue and is not yet targeted by other multiple sclerosis therapies."],["dc.description.sponsorship","Biogen Idec; Ruhr University Bochum"],["dc.identifier.doi","10.1093/brain/awq386"],["dc.identifier.isi","000287745100006"],["dc.identifier.pmid","21354971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23784"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","217"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Stegbauer, Johannes"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.date.accessioned","2018-11-07T11:21:07Z"],["dc.date.available","2018-11-07T11:21:07Z"],["dc.date.issued","2009"],["dc.description.abstract","In the recent years, it has become increasingly clear that the immune response is also influenced by mediators which were first discovered as regulators in the nervous or also cardiovascular system. Here, small peptide hormones may play an important role. Kinins like bradykinins act on the endothelium and play a role for trafficking of lymphocytes over the blood-brain barrier. Neuropeptides like vasoactive intestinal peptide or neuropeptide Y also directly act on T cells and favour the differentiation of Th2 cells or regulatory T cell populations. Recently, the renin-angiotensin system (RAS) came into the focus of interest. Inhibition of the RAS at different levels may influence autoimmune responses and involve T cells as well as antigen-presenting cells, probably via different signalling pathways. Inhibitors of angiotensin converting enzyme and antagonists of the angiotensin I receptors are used in the treatment of hypertension, kidney disease or stroke by millions of people worldwide. These inexpensive and safe pharmaceuticals may also represent an interesting and innovative approach for the (combination) treatment of autoimmune diseases like multiple sclerosis. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2009.08.008"],["dc.identifier.isi","000272896700001"],["dc.identifier.pmid","19748684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55698"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Small but powerful: Short peptide hormones and their role in autoimmune inflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2248"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2263"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Demir, Seray"],["dc.contributor.author","Wiese, Stefan"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Siglienti, Ines"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Neumann, Harald"],["dc.contributor.author","Sendtner, Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T08:40:38Z"],["dc.date.available","2018-11-07T08:40:38Z"],["dc.date.issued","2010"],["dc.description.abstract","Brain-derived neurotrophic factor plays a key role in neuronal and axonal survival. Brain-derived neurotrophic factor is expressed in the immune cells in lesions of experimental autoimmune encephalomyelitis and multiple sclerosis, thus potentially mediating neuroprotective effects. We investigated the functional role of brain-derived neurotrophic factor in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Mice deficient for brain-derived neurotrophic factor in immune cells displayed an attenuated immune response in the acute phase of experimental autoimmune encephalomyelitis, but progressive disability with enhanced axonal loss in the chronic phase of the disease. In mice deficient for central nervous system-derived brain-derived neurotrophic factor via glial fibrillary acidic protein-crescentin-mediated deletion, a more severe course of experimental autoimmune encephalomyelitis and an overall increased axonal loss was observed. In a lentiviral approach, injection of brain-derived neurotrophic factor-overexpressing T cells led to a less severe course of experimental autoimmune encephalomyelitis and direct axonal protection. Our data imply a functional role of brain-derived neurotrophic factor in autoimmune demyelination by mediating axon protection."],["dc.identifier.doi","10.1093/brain/awq179"],["dc.identifier.isi","000280982700010"],["dc.identifier.pmid","20826430"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6203"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19277"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Functional role of brain-derived neurotrophic factor in neuroprotective autoimmunity: therapeutic implications in a model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1604"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1606"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","Chan, Andrew"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Linker, Ralf"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:57:12Z"],["dc.date.available","2018-11-07T10:57:12Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1007/s00415-007-0593-9"],["dc.identifier.isi","000251096000021"],["dc.identifier.pmid","17713826"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50186"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Rescue therapy with anti-CD20 treatment in neuroimmunologic breakthrough disease"],["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"]]

[["dc.bibliographiccitation.firstpage","363"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","364"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Schroeder, S. D."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Waschbisch, Anne"],["dc.date.accessioned","2018-11-07T09:05:36Z"],["dc.date.available","2018-11-07T09:05:36Z"],["dc.date.issued","2012"],["dc.identifier.isi","000328702202174"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25362"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Lyon, FRANCE"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Non-classical and intermediate monocytes in relapsing-remitting 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","247"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","258"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Geyer, Eva"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T09:13:35Z"],["dc.date.available","2018-11-07T09:13:35Z"],["dc.date.issued","2012"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) is involved in neuronal and glial development and survival. While neurons and astrocytes are its main cellular source in the central nervous system (CNS), bioactive BDNF is also expressed in immune cells and in lesions of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Previous data revealed that BDNF exerts neuroprotective effects in myelin oligodendrocyte glycoprotein-induced EAE. Using a conditional knock-out model with inducible deletion of BDNF, we here show that clinical symptoms and structural damage are increased when BDNF is absent during the initiation phase of clinical EAE. In contrast, deletion of BDNF later in the disease course of EAE did not result in significant changes, either in the disease course or in axonal integrity. Bone marrow chimeras revealed that the deletion of BDNF in the CNS alone, with no deletion of BDNF in the infiltrating immune cells, was sufficient for the observed effects. Finally, the therapeutic effect of glatiramer acetate, a well-characterized disease-modifying drug with the potential to modulate BDNF expression, was partially reversed in mice in which BDNF was deleted shortly before the onset of disease. In summary, our data argue for an early window of therapeutic opportunity where modulation of BDNF may exert neuroprotective effects in experimental autoimmune demyelination."],["dc.identifier.doi","10.1007/s00401-011-0890-3"],["dc.identifier.isi","000301855900008"],["dc.identifier.pmid","22009304"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27216"],["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","Central nervous system rather than immune cell-derived BDNF mediates axonal protective effects early in autoimmune demyelination"],["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.firstpage","1326"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1338"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Flach, Anne-Christine"],["dc.contributor.author","Litke, Tanja"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Lingner, Thomas"],["dc.contributor.author","Bommhardt, Ursula"],["dc.contributor.author","Sendtner, Michael"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Fluegel, Alexander"],["dc.contributor.author","Luehder, Fred"],["dc.date.accessioned","2018-11-07T09:57:51Z"],["dc.date.available","2018-11-07T09:57:51Z"],["dc.date.issued","2015"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) promotes neuronal survival, regeneration, and plasticity. Emerging evidence also indicates an essential role for BDNF outside the nervous system, for instance in immune cells. We therefore investigated the impact of BDNF on Tcells using BDNF knockout (KO) mice and conditional KO mice lacking BDNF specifically in this lymphoid subset. In both settings, we observed diminished T-cell cellularity in peripheral lymphoid organs and an increase in CD4(+)CD44(+) memory Tcells. Analysis of thymocyte development revealed diminished total thymocyte numbers, accompanied by a significant increase in CD4/CD8 double-negative (DN) thymocytes due to a partial block in the transition from the DN3 to the DN4 stage. This was neither due to increased thymocyte apoptosis nor defects in the expression of the TCR- chain or the pre-TCR. In contrast, pERK but not pAKT levels were diminished in DN3 BDNF-deficient thymocytes. BDNF deficiency in Tcells did not result in gross deficits in peripheral acute immune responses nor in changes of the homeostatic proliferation of peripheral Tcells. Taken together, our data reveal a critical autocrine and/or paracrine role of T-cell-derived BDNF in thymocyte maturation involving ERK-mediated TCR signaling pathways."],["dc.identifier.doi","10.1002/eji.201444985"],["dc.identifier.isi","000354182300006"],["dc.identifier.pmid","25627579"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37248"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.title","Thymocyte-derived BDNF influences T-cell maturation at the DN3/DN4 transition stage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","38"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","42"],["dc.bibliographiccitation.volume","246"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Kubera, Katharina"],["dc.contributor.author","Rosenthal, Bastian"],["dc.contributor.author","Kaltschmidt, Barbara"],["dc.contributor.author","Kaltschmidt, Christian"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T09:10:25Z"],["dc.date.available","2018-11-07T09:10:25Z"],["dc.date.issued","2012"],["dc.description.abstract","Neuro-axonal damage is a major hallmark of multiple sclerosis (MS). To date, not much is known on the underlying mechanisms of neuronal degeneration. In disease model myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE), there is a significant loss of alpha motorneurons in the cervical as well as thoracic and lumbar spinal cord. We further investigate the role of activated NF-kappa B for neuronal damage in a conditional ablation mouse model. A calcium calmodulin kinase II promoter-driven tetracycline transactivator is employed to regulate the expression of a human transdominant negative I kappa B-alpha mutant in the basal forebrain and selected neuronal subpopulations in the cerebellum and spinal cord including cerebellar Purkinje cells and spinal cord alpha motorneurons. In these mice with conditional neuronal NF-kappa B ablation, the clinical course of MOG-EAE, parameters of inflammation and axonal densities in the spinal cord white and grey matter as well as numbers of alpha motorneurons are not different to littermate controls. In conclusion, neuronal NF-kappa B ablation does not modulate neurodegeneration in autoimmune demyelination. (C) 2012 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","University of Gottingen, Germany"],["dc.identifier.doi","10.1016/j.jneuroim.2012.03.005"],["dc.identifier.isi","000304026900006"],["dc.identifier.pmid","22475633"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26485"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Neuronal NF-kappa B ablation does not influence neuro-axonal degeneration in experimental autoimmune demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","49"],["dc.bibliographiccitation.journal","Molecular Neurodegeneration"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Heidecke, Harald"],["dc.contributor.author","Schroeder, Alexandra"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Wachter, R. Rolf"],["dc.contributor.author","Hoffmann, Rainer"],["dc.contributor.author","Ellrichmann, Gisa"],["dc.contributor.author","Dragun, Duska"],["dc.contributor.author","Waschbisch, Anne"],["dc.contributor.author","Stegbauer, Johannes"],["dc.contributor.author","Klotz, Peter"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Dechend, Ralf"],["dc.contributor.author","Mueller, Dominik N."],["dc.contributor.author","Saft, Carsten"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2018-11-07T09:32:37Z"],["dc.date.available","2018-11-07T09:32:37Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: In the recent years, a role of the immune system in Huntington's disease (HD) is increasingly recognized. Here we investigate the presence of T cell activating auto-antibodies against angiotensin II type 1 receptors (AT1R) in all stages of the disease as compared to healthy controls and patients suffering from multiple sclerosis (MS) as a prototype neurologic autoimmune disease. Results: As compared to controls, MS patients show higher titers of anti-AT1R antibodies, especially in individuals with active disease. In HD, anti-AT1R antibodies are more frequent than in healthy controls or even MS and occur in 37.9% of patients with relevant titers >= 20 U/ml. In a correlation analysis with clinical parameters, the presence of AT1R antibodies in the sera of HD individuals inversely correlated with the age of onset and positively with the disease burden score as well as with smoking and infection. Conclusions: These data suggest a dysfunction of the adaptive immune system in HD which may be triggered by different stimuli including autoimmune responses, infection and possibly also smoking."],["dc.description.sponsorship","German Research Council [DFG Exc 257]; Novartis foundation"],["dc.identifier.doi","10.1186/1750-1326-9-49"],["dc.identifier.isi","000345934100001"],["dc.identifier.pmid","25398321"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11123"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31790"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1750-1326"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Increase of angiotensin II type 1 receptor auto-antibodies in Huntington's disease"],["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.firstpage","96"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","98"],["dc.bibliographiccitation.volume","385"],["dc.contributor.author","Olmes, David G."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lee, De-Hyung"],["dc.contributor.author","Rosenwald, Andreas"],["dc.contributor.author","Doerfler, Arnd"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Linker, Ralf A."],["dc.date.accessioned","2020-12-10T14:25:15Z"],["dc.date.available","2020-12-10T14:25:15Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.jns.2017.12.021"],["dc.identifier.issn","0022-510X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72500"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","CLIPPERS with longitudinally extensive transverse myelitis: Role of T versus B cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]