Kruse, Niels

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Selmaj, K."],["dc.date.accessioned","2018-11-07T10:46:03Z"],["dc.date.available","2018-11-07T10:46:03Z"],["dc.date.issued","2004"],["dc.format.extent","158"],["dc.identifier.isi","000224003200531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47653"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Multiple sclerosis: impaired phenotype and maturation of plasmacytoid dendritic cells"],["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"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Selmaj, K."],["dc.date.accessioned","2018-11-07T10:56:30Z"],["dc.date.available","2018-11-07T10:56:30Z"],["dc.date.issued","2005"],["dc.format.extent","S121"],["dc.identifier.isi","000232249900443"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50026"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hodder Arnold, Hodder Headline Plc"],["dc.publisher.place","London"],["dc.relation.conference","21st Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis/10th Annual Meeting of Rehabilitation in MS"],["dc.relation.eventlocation","Thessaloniki, GREECE"],["dc.relation.issn","1352-4585"],["dc.title","Impaired reaction of plasmacytoid dendritic cells to toll-like receptor 7 and 9 ligands in MS patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Kroner, Antje"],["dc.contributor.author","Rosche, B."],["dc.contributor.author","Kolb-Maurer, A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Rieckmann, Peter"],["dc.contributor.author","Maurer, M."],["dc.date.accessioned","2018-11-07T10:46:02Z"],["dc.date.available","2018-11-07T10:46:02Z"],["dc.date.issued","2004"],["dc.format.extent","24"],["dc.identifier.isi","000224003200077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47651"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Analysis of the Asp299Gly polymorphism in the Toll-like receptor 4 (TLR-4) gene in patients with 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","70"],["dc.bibliographiccitation.journal","Journal of Immunological Methods"],["dc.bibliographiccitation.lastpage","75"],["dc.bibliographiccitation.volume","426"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2018-11-07T09:49:17Z"],["dc.date.available","2018-11-07T09:49:17Z"],["dc.date.issued","2015"],["dc.description.abstract","The quantification of a-Synuclein in cerebrospinal fluid (CSF) as a biornarker has gained tremendous interest in the last years. Several commercially available immunoassays are emerging. We here describe the full validation of one commercially available ELISA assay for the quantification of a-Synuclein in human CSF (Covance alpha-Synuclein ELISA kit). The study was conducted within the BIOMARKAPD project in the European initiative Joint Program for Neurodegenerative Diseases (JPND). We investigated the effect of several pre-analytical and analytical confounders: i.e. (1) need for centrifugation of freshly drawn CSF, (2) sample stability, (3) delay of freezing, (4) volume of storage aliquots, (5) freeze/thaw cycles, (6) thawing conditions, (7) dilution linearity, (8) parallelism, (9) spike recovery, and (10) precision. None of these confounders influenced the levels of alpha-Synuclein in CSF significantly. We found a very high intra-assay precision. The inter-assay precision was lower than expected due to different performances of kit lots used. Overall the validated immunoassay is useful for the quantification of alpha-Synuclein in human CSF. (C) 2015 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","JPND"],["dc.identifier.doi","10.1016/j.jim.2015.08.003"],["dc.identifier.isi","000366079800010"],["dc.identifier.pmid","26271436"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35478"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-7905"],["dc.relation.issn","0022-1759"],["dc.title","Validation of a commercially available enzyme-linked immunoabsorbent assay for the quantification of human alpha-Synuclein in cerebrospinal fluid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","481"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Stuendl, Anne"],["dc.contributor.author","Kunadt, Marcel"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Danzer, Karin M."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schneider, Anja"],["dc.date.accessioned","2018-11-07T10:18:37Z"],["dc.date.available","2018-11-07T10:18:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Extracellular alpha-synuclein has been proposed as a crucial mechanism for induction of pathological aggregate formation in previously healthy cells. In vitro, extracellular alpha-synuclein is partially associated with exosomal vesicles. Recently, we have provided evidence that exosomal alpha-synuclein is present in the central nervous system in vivo. We hypothesized that exosomal alpha-synuclein species from patients with alpha-synuclein related neurodegeneration serve as carriers for interneuronal disease transmission. We isolated exosomes from cerebrospinal fluid from patients with Parkinson's disease, dementia with Lewy bodies, progressive supranuclear palsy as a non-alpha-synuclein related disorder that clinically overlaps with Parkinson's disease, and neurological controls. Cerebrospinal fluid exosome numbers, alpha-synuclein protein content of cerebrospinal fluid exosomes and their potential to induce oligomerization of alpha-synuclein were analysed. The quantification of cerebrospinal fluid exosomal alpha-synuclein showed distinct differences between patients with Parkinson's disease and dementia with Lewy bodies. In addition, exosomal alpha-synuclein levels correlated with the severity of cognitive impairment in cross-sectional samples from patients with dementia with Lewy bodies. Importantly, cerebrospinal fluid exosomes derived from Parkinson's disease and dementia with Lewy bodies induce oligomerization of alpha-synuclein in a reporter cell line in a dose-dependent manner. Our data suggest that cerebrospinal fluid exosomes from patients with Parkinson's disease and dementia with Lewy bodies contain a pathogenic species of alpha-synuclein, which could initiate oligomerization of soluble alpha-synuclein in target cells and confer disease pathology."],["dc.identifier.doi","10.1093/brain/awv346"],["dc.identifier.isi","000370205100026"],["dc.identifier.pmid","26647156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41483"],["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","Induction of alpha-synuclein aggregate formation by CSF exosomes from patients with Parkinson's disease and dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","277"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","279"],["dc.bibliographiccitation.volume","278"],["dc.contributor.author","Grey (nee Cotte), Steffi"],["dc.contributor.author","Salmen (nee Stroet), Anke"],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Starck, Michaela"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Comabella, Manuel"],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Fleischer, Vinzenz"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2018-11-07T10:02:07Z"],["dc.date.available","2018-11-07T10:02:07Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Mitoxantrone is used on an off-label basis in primary progressive MS (PPMS).ABC-transporter-genotypes are associated with therapeutic response in relapsing/secondary progressive MS (RP/SPMS). Objective: To evaluate potential pharmacogenetic response markers for mitoxantrone in PPMS. Methods: 41 mitoxantrone-treated PPMS-patients, 155 mitoxantrone-treated RP/SPMS-patients and 43 PPMS-controls were retrospectively assessed for clinical therapy-response and in correlation with four single-nucleotide-polymorphisms in ABCB1- and ABCG2-genes. Results: 53.7% PPMS-patients were mitoxantrone-responders, in comparison to 78.1% of RP/SPMS-patients (p = 0.039). There was no association between genotype and treatment response. Conclusion: Our data discourages the use of mitoxantrone in PPMS regardless of pharmacogenetic response markers previously described in RP/SPMS. (C) 2014 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2014.11.017"],["dc.identifier.isi","000349269300035"],["dc.identifier.pmid","25468777"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38167"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Lack of efficacy of mitoxantrone in primary progressive Multiple Sclerosis irrespective of pharmacogenetic factors: A multi-center, retrospective analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","814"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuropathology and Applied Neurobiology"],["dc.bibliographiccitation.lastpage","831"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Haeusler, Darius"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2018-11-07T09:50:34Z"],["dc.date.available","2018-11-07T09:50:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Aims: Natalizumab is a humanized monoclonal antibody specific for CD49d receptors of integrins. It inhibits the entry of inflammatory cells into the central nervous system and is approved for the treatment of relapsing-remitting multiple sclerosis (MS). Several lines of evidence indicate an involvement of B cells and plasma cells in MS pathogenesis. However, treatment with the natalizumab analogon PS/2 immunoglobulin G (IgG) has so far only been investigated in T cell-mediated animal models of MS. Due to the importance of B lineage cells in the pathogenesis of MS, the objective of the present study has thus been to analyse the effects of PS/2 IgG in a mouse model of MS with T and B cell cooperation (OSE mice). Methods: OSE mice were treated with the natalizumab analogon PS/2 IgG either at disease onset or after peak of disease. Treatment was also performed with PS/2 F(ab')2 fragments. Results: PS/2 IgG treatment improved the clinical outcome and decreased spinal cord demyelination and immune cell infiltration if given early in the disease course. Treatment increased blood leukocytes and resulted in a partial internalization of CD49d in T and B cells. The therapeutic effects of PS/2 IgG injections were independent of the Fc fragment as F(ab') 2 injections were equally beneficial. In contrast, PS/2 IgG was not effective when given late in the disease course. Conclusions: Results indicate that natalizumab may also be beneficial in MS with B cell-driven immunopathogenesis."],["dc.description.sponsorship","DFG Transregional Collaborative Research Group [TRR-SFB 43]"],["dc.identifier.doi","10.1111/nan.12220"],["dc.identifier.isi","000364640500008"],["dc.identifier.pmid","25641089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35732"],["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","Natalizumab analogon therapy is effective in a B cell-dependent multiple sclerosis model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1462"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Brain: A Journal of Neurology"],["dc.bibliographiccitation.lastpage","1475"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Arotcarena, Marie-Laure"],["dc.contributor.author","Dovero, Sandra"],["dc.contributor.author","Prigent, Alice"],["dc.contributor.author","Bourdenx, Mathieu"],["dc.contributor.author","Camus, Sandrine"],["dc.contributor.author","Porras, Gregory"],["dc.contributor.author","Thiolat, Marie-Laure"],["dc.contributor.author","Tasselli, Maddalena"],["dc.contributor.author","Aubert, Philippe"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trigo Damas, Ines"],["dc.contributor.author","Estrada, Cristina"],["dc.contributor.author","Garcia-Carrillo, Nuria"],["dc.contributor.author","Vaikath, Nishant N"],["dc.contributor.author","El-Agnaf, Omar M A"],["dc.contributor.author","Herrero, Maria Trinidad"],["dc.contributor.author","Vila, Miquel"],["dc.contributor.author","Obeso, Jose A"],["dc.contributor.author","Derkinderen, Pascal"],["dc.contributor.author","Dehay, Benjamin"],["dc.contributor.author","Bezard, Erwan"],["dc.date.accessioned","2021-04-14T08:26:41Z"],["dc.date.available","2021-04-14T08:26:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/brain/awaa096"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82041"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Bidirectional gut-to-brain and brain-to-gut propagation of synucleinopathy in non-human primates"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Selmaj, K."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:48:35Z"],["dc.date.available","2018-11-07T10:48:35Z"],["dc.date.issued","2004"],["dc.format.extent","43"],["dc.identifier.isi","000222500400152"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48231"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.publisher.place","Darmstadt"],["dc.relation.conference","14th Meeting of the European-Neurological-Society"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","0340-5354"],["dc.title","Altered regulatory function of plasmacytoid dendritic cells in 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","123"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cellular Immunology"],["dc.bibliographiccitation.lastpage","130"],["dc.bibliographiccitation.volume","237"],["dc.contributor.author","Hofstetter, Harald H."],["dc.contributor.author","Ibrahim, S. M."],["dc.contributor.author","Koczan, D."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Weishaupt, Andreas"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:55:11Z"],["dc.date.available","2018-11-07T10:55:11Z"],["dc.date.issued","2005"],["dc.description.abstract","Experimental autoimmune encephalomyelitis (EAE) is widely regarded as an animal model of the human disease multiple sclerosis. A multitude of studies has investigated the neuroantigen-specific T-cell mediated cytokine pattern present in animals with EAE. In particular, the role of the so-called Th1- and Th2-cytokines has been addressed. In a recent study.. it has been demonstrated that IL-23 rather than IL-12 is critical for modulating the character of the developing immune response towards a proinflammatory response and leading to EAE. IL-17 is a crucial effector cytokine, whose production is specifically triggered by IL-23, and it has been shown to be an essential,,g inflammatory mediator in other autoimmune diseases and inflammatory conditions. This led us to investigate the role of IL-17 in EAE. Strong antigen-specific production of IL-17 was demonstrated both in peripheral immune organs and in the CNS in acute and chronic EAE, as demonstrated by ELISPOT and RT-PCR analysis. Therapeutic neutralization of IL-17 with IL-17-receptor-Fc-protein in acute EAE ameliorated clinical symptoms. Neutralization of IL-17 with a monoclonal antibody also ameliorated the disease course. We conclude that IL-17 is crucially involved in the cytokine network as an effector cytokine in EAE. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.cellimm.2005.11.002"],["dc.identifier.isi","000235248700006"],["dc.identifier.pmid","16386239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49727"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0008-8749"],["dc.title","Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]