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","126"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","149"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bowman, Frederick DuBois"],["dc.contributor.author","Drake, Daniel"],["dc.contributor.author","Duong, Jimmy"],["dc.contributor.author","Blennow, Kaj"],["dc.contributor.author","El‐Agnaf, Omar"],["dc.contributor.author","Shaw, Leslie M."],["dc.contributor.author","Masucci, Jennifer"],["dc.contributor.author","Taylor, Peggy"],["dc.contributor.author","Umek, Robert M."],["dc.contributor.author","Dunty, Jill M."],["dc.contributor.author","Smith, Chris L."],["dc.contributor.author","Stoops, Erik"],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","Schmid, Adrian W."],["dc.contributor.author","Moniatte, Marc"],["dc.contributor.author","Zhang, Jing"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Lashuel, Hilal A."],["dc.contributor.author","Teunissen, Charlotte"],["dc.contributor.author","Schubert, Tanja"],["dc.contributor.author","Dave, Kuldip D."],["dc.contributor.author","Hutten, Samantha J."],["dc.contributor.author","Zetterberg, Henrik"],["dc.date.accessioned","2019-07-09T11:50:53Z"],["dc.date.available","2019-07-09T11:50:53Z"],["dc.date.issued","2019"],["dc.description.abstract","α-Synuclein is the major component of Lewy bodies and a candidate biomarker for neurodegenerative diseases in which Lewy bodies are common, including Parkinson's disease and dementia with Lewy bodies. A large body of literature suggests that these disorders are characterized by reduced concentrations of α-synuclein in cerebrospinal fluid (CSF), with overlapping concentrations compared to healthy controls and variability across studies. Several reasons can account for this variability, including technical ones, such as inter-assay and inter-laboratory variation (reproducibility). We compared four immunochemical methods for the quantification of α-synuclein concentration in 50 unique CSF samples. All methods were designed to capture most of the existing α-synuclein forms in CSF ('total' α-synuclein). Each of the four methods showed high analytical precision, excellent correlation between laboratories (R2 0.83-0.99), and good correlation with each other (R2 0.64-0.93), although the slopes of the regression lines were different between the four immunoassays. The use of common reference CSF samples decreased the differences in α-synuclein concentration between detection methods and technologies. Pilot data on an immunoprecipitation mass spectrometry (IP-MS) method is also presented. Our results suggest that the four immunochemical methods and the IP-MS method measure similar forms of α-synuclein and that a common reference material would allow harmonization of results between immunoassays."],["dc.identifier.doi","10.1111/jnc.14569"],["dc.identifier.pmid","30125936"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59849"],["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.subject.ddc","610"],["dc.title","Antibody‐based methods for the measurement of α‐synuclein concentration in human cerebrospinal fluid – method comparison and round robin study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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","2517"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2530"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Cotte, S."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Huber, B."],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl, Uwe K."],["dc.contributor.author","Starck, Michaela"],["dc.contributor.author","Koenig, N."],["dc.contributor.author","Tellez, N."],["dc.contributor.author","Doerr, J."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Koepsell, Hermann"],["dc.contributor.author","Pannek, H."],["dc.contributor.author","Montalban, Xavier"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, A."],["dc.date.accessioned","2018-11-07T11:24:34Z"],["dc.date.available","2018-11-07T11:24:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Escalation therapy with mitoxantrone (MX) in highly active multiple sclerosis is limited by partially dose-dependent side-effects. Predictors of therapeutic response may result in individualized risk stratification and MX dosing. ATP-binding cassette-transporters ABCB1 and ABCG2 represent multi-drug resistance mechanisms involved in active cellular MX efflux. Here, we investigated the role of ABC-gene single nucleotide polymorphisms (SNPs) for clinical MX response, corroborated by experimental in vitro and in vivo data. Frequencies of ABCB1 2677GT, 3435CT and five ABCG2-SNPs were analysed in 832 multiple sclerosis patients (Germany, Spain) and 264 healthy donors. Using a flow-cytometry-based in vitro assay, MX efflux in leukocytes from individuals with variant alleles in both ABC-genes (designated genotype ABCB1/ABCG2-L(ow), 22.2 of patients) was 37.7 lower than from individuals homozygous for common alleles (ABCB1/ABCG2-H(igh), P 0.05, 14.8 of patients), resulting in genotype-dependent MX accumulation and cell death. Addition of glucocorticosteroids (GCs) inhibited MX efflux in vitro. ABC-transporters were highly expressed in leukocyte subsets, glial and neuronal cells as well as myocardium, i.e. cells/tissues potentially affected by MX therapy. In vivo significance was further corroborated in experimental autoimmune encephalomyelitis in Abcg2(/) animals. Using a MX dose titrated to be ineffective in wild-type animals, disease course and histopathology in Abcg2(/) mice were strongly ameliorated. Retrospective clinical analysis in MX monotherapy patients (n 155) used expanded disability status scale, relapse rate and multiple sclerosis functional composite as major outcome parameters. The clinical response rate [overall 121 of 155 patients (78.1)] increased significantly with genotypes associated with decreasing ABCB1/ABCG2-function [ABCB1/ABCG2-H 15/24 (62.5) responders, ABCB1/ABCG2-I(ntermediate) 78/98 (79.6), ABCB1/ABCG2-L 28/33 (84.8), exact Cochran-Armitage test P 0.039]. The odds ratio for response was 1.9 (95 CI 1.03.5) with each increase in ABCB1/ABCG2 score (from ABCB1/ABCG2-H to I-, and I to L). In 36 patients with severe cardiac or haematological side effects no statistically relevant difference in genotype frequency was observed. However, one patient with biopsy proven cardiomyopathy only after 24 mg/m(2) MX exhibited a rare genotype with variant, partly homozygous alleles in 3 ABC-transporter genes. In conclusion, SNPs in ABC-transporter genes may serve as pharmacogenetic markers associated with clinical response to MX therapy in multiple sclerosis. Combined MX/GC-treatment warrants further investigation."],["dc.description.sponsorship","Merck Serono, Germany"],["dc.identifier.doi","10.1093/brain/awp164"],["dc.identifier.isi","000269963600021"],["dc.identifier.pmid","19605531"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6073"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56436"],["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","ABC-transporter gene-polymorphisms are potential pharmacogenetic markers for mitoxantrone response in 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","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"]]