Nessler, Stefan

[["dc.bibliographiccitation.firstpage","19057"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","19062"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Zhou, D."],["dc.contributor.author","Srivastava, Rajneesh"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Grummel, Verena"],["dc.contributor.author","Sommer, Norbert"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T08:51:00Z"],["dc.date.available","2018-11-07T08:51:00Z"],["dc.date.issued","2006"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Although the cause of MS is still uncertain, many findings point toward an ongoing autoimmune response to myelin antigens. Because of its location on the outer surface of the myelin sheath and its pathogenicity in the experimental autoimmune encephalomyelitis model, myelin oligodendrocyte glycoprotein (MOG) is one of the potential disease-causing self antigens in MS. However, the role of MOG in the pathogenesis of MS has remained controversial. In this study we addressed the occurrence of autoantibodies to native MOG and its implication for demyelination and axonal loss in MS. We applied a high-sensitivity bioassay, which allowed detecting autoantibodies that bind to the extracellular part of native MOG. Antibodies, mostly IgG, were found in sera that bound with high affinity to strictly conformational epitopes of the extracellular domain of MOG. IgG but not IgM antibody titers to native MOG were significantly higher in MS patients compared with different control groups with the highest prevalence in primary progressive MS patients. Serum autoantibodies to native MOG induced death of MOG-expressing target cells in vitro. Serum from MS patients with high anti-MOG antibody titers stained white matter myelin in rat brain and enhanced demyelination and axonal damage when transferred to autoimmune encephalomyelitis animals. Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients."],["dc.identifier.doi","10.1073/pnas.0607242103"],["dc.identifier.isi","000242884200034"],["dc.identifier.pmid","17142321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein 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","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","179"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bittner, Alwina"],["dc.contributor.author","Schlegel, Kerstin"],["dc.contributor.author","Gronen, Felix"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Sommer, Norbert"],["dc.date.accessioned","2018-11-07T09:11:30Z"],["dc.date.available","2018-11-07T09:11:30Z"],["dc.date.issued","2006"],["dc.description.abstract","Substance P (SP) is an excitatory neurotransmitter in the central and peripheral nervous system. Most of its physiological functions are mediated through binding to the neurokinin-1 receptor (NK-1R). Recently, proinflammatory properties of SP have been described. In this study we utilized T cell transfer experimental autoimmune encephalomyelitis (EAE) to investigate the role of SP in CNS autoimmune disease. Treatment with the NK-1R antagonist CP-96,345 dramatically reduced clinical and histological signs of EAE if administered before disease onset. The protective effect of CP96,345 treatment was related to a reduced expression of the adhesion molecules ICAM-1 and VCAM-1 on CNS endothelia. The cellular composition or activation status of splenocytes was not affected by CP-96,345 administration, while the secretion of proinflammatory Thl cytokines was reduced in treated animals. Th2 cytokines remained largely unaffected by NK-1 receptor antagonist treatment. In summary, our findings suggest that the protective effect of CP96,345 treatment is mediated by stabilization of the blood-brain barrier and suppression of Thl immunity. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.06.026"],["dc.identifier.isi","000241821800001"],["dc.identifier.pmid","16904192"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26735"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Suppression of autoimmune encephalomyelitis by a neurokinin-1 receptor antagonist - A putative role for substance P in CNS inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S276"],["dc.bibliographiccitation.journal","European Journal of Nuclear Medicine and Molecular Imaging"],["dc.bibliographiccitation.lastpage","S277"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Lapa, Constantin"],["dc.contributor.author","Buck, D."],["dc.contributor.author","Foerschler, Annette"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Wester, H."],["dc.contributor.author","Korn, Thomas"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Jacobi, Heike"],["dc.contributor.author","Zimmer, C."],["dc.contributor.author","Schwaiger, M."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Krause, B."],["dc.date.accessioned","2018-11-07T08:38:09Z"],["dc.date.available","2018-11-07T08:38:09Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283023800350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","1619-7070"],["dc.title","Molecular small animal imaging in an Experimental Autoimmune Encephalomyelitis (EAE) rat model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","617"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","629"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Lam, Chiwah"],["dc.contributor.author","Kalluri, Sudhakar Reddy"],["dc.contributor.author","Saikali, Philippe"],["dc.contributor.author","Bautista, Katherine"],["dc.contributor.author","Dupree, Cecily"],["dc.contributor.author","Glogowska, Magdalena"],["dc.contributor.author","Case, David"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Owens, Gregory P."],["dc.contributor.author","Gilden, Donald H."],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T11:22:20Z"],["dc.date.available","2018-11-07T11:22:20Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The serum of most neuromyelitis optica (NMO) patients contains autoantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of the brain. Our objectives were to determine the source of central nervous system (CNS) NMO-IgGs and their role in disease pathogenesis. Methods: Fluorescence-activated cell sorting and single-cell reverse transcriptase polymerase chain reaction were used to identify overrepresented plasma cell immunoglobulin (Ig) sequences in the cerebrospinal fluid (CSF) of an NMO patient after a first clinical attack. Monoclonal recombinant antibodies (rAbs) were generated from the paired heavy and light chain sequences and tested for target specificity and Fc effector function. The effect of CSF rAbs on CNS immunopathology was investigated by delivering single rAbs to rats with experimental autoimmune encephalomyelitis (EAE). Results: Repertoire analysis revealed a dynamic, clonally expanded plasma cell population with features of an antigen-targeted response. Using multiple independent assays, 6 of 11 rAbs generated from CSF plasma cell clones specifically bound to AQP4. AQP4-specific rAbs recognized conformational epitopes and mediated both AQP4-directed antibody-dependent cellular cytotoxicity and complement-mediated lysis. When administered to rats with EAE, an AQP4-specific NMO CSF rAb induced NMO immunopathology: perivascular astrocyte depletion, myelinolysls, and complement and Ig deposition. Interpretation: Molecular characterization of the CSF plasma cell repertoire in an early NMO patient demonstrates that AQP4-specfic Ig is synthesized intrathecally at disease onset and directly contributes to CNS pathology. AQP4 is now the first confirmed antigenic target in human demyelinating disease."],["dc.identifier.doi","10.1002/ana.21802"],["dc.identifier.isi","000272314500010"],["dc.identifier.pmid","19938104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55976"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","Intrathecal Pathogenic Anti-Aquaporin-4 Antibodies in Early Neuromyelitis Optica"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Bittner, A."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Sommer, N."],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T10:56:29Z"],["dc.date.available","2018-11-07T10:56:29Z"],["dc.date.issued","2005"],["dc.identifier.isi","000232249900170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50022"],["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.title","MRI-histopathology correlation in a clonal mouse EAE model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Bennett, Jeffrey L."],["dc.contributor.author","Lam, Carolyn S. P."],["dc.contributor.author","Kalluri, Sudhakar Reddy"],["dc.contributor.author","Saikali, Philippe"],["dc.contributor.author","Bautista, K."],["dc.contributor.author","Dupree, Cecily"],["dc.contributor.author","Glogowska, Magdalena"],["dc.contributor.author","Case, David"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Owens, Gregory P."],["dc.contributor.author","Gilden, Donald H."],["dc.contributor.author","Nessler, S."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T11:25:12Z"],["dc.date.available","2018-11-07T11:25:12Z"],["dc.date.issued","2009"],["dc.format.extent","S74"],["dc.identifier.isi","000269652500215"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56577"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","Pathogenic anti-aquaporin-4 antibodies are produced by intrathecal clonally-expanded plasma cells in early neuromyelitis optica"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","375"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","388"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Hu, Wei"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Eagar, Todd N."],["dc.contributor.author","Kane, Lawrence P."],["dc.contributor.author","Leliveld, S. Rutger"],["dc.contributor.author","Mueller-Schiffmann, Andreas"],["dc.contributor.author","Gocke, Anne R."],["dc.contributor.author","Lovett-Racke, Amy"],["dc.contributor.author","Ben, Li-Hong"],["dc.contributor.author","Hussain, Rehana Z."],["dc.contributor.author","Breil, Andreas"],["dc.contributor.author","Elliott, Jeffrey L."],["dc.contributor.author","Puttaparthi, Krishna"],["dc.contributor.author","Cravens, Petra D."],["dc.contributor.author","Singh, Mahendra P."],["dc.contributor.author","Petsch, Benjamin"],["dc.contributor.author","Stitz, Lothar"],["dc.contributor.author","Racke, Michael K."],["dc.contributor.author","Korth, Carsten"],["dc.contributor.author","Stuve, Olaf"],["dc.date.accessioned","2018-11-07T08:46:03Z"],["dc.date.available","2018-11-07T08:46:03Z"],["dc.date.issued","2010"],["dc.description.abstract","The primary biological function of the endogenous cellular prion protein has remained unclear. We investigated its biological function in the generation of cellular immune responses using cellular prion protein gene-specific small interfering ribonucleic acid in vivo and in vitro. Our results were confirmed by blocking cellular prion protein with monovalent antibodies and by using cellular prion protein-deficient and -transgenic mice. In vivo prion protein gene-small interfering ribonucleic acid treatment effects were of limited duration, restricted to secondary lymphoid organs and resulted in a 70% reduction of cellular prion protein expression in leukocytes. Disruption of cellular prion protein signalling augmented antigen-specific activation and proliferation, and enhanced T cell receptor signalling, resulting in zeta-chain-associated protein-70 phosphorylation and nuclear factor of activated T cells/activator protein 1 transcriptional activity. In vivo prion protein gene-small interfering ribonucleic acid treatment promoted T cell differentiation towards pro-inflammatory phenotypes and increased survival of antigen-specific T cells. Cellular prion protein silencing with small interfering ribonucleic acid also resulted in the worsening of actively induced and adoptively transferred experimental autoimmune encephalomyelitis. Finally, treatment of myelin basic protein(1-11) T cell receptor transgenic mice with prion protein gene-small interfering ribonucleic acid resulted in spontaneous experimental autoimmune encephalomyelitis. Thus, central nervous system autoimmune disease was modulated at all stages of disease: the generation of the T cell effector response, the elicitation of T effector function and the perpetuation of cellular immune responses. Our findings indicate that cellular prion protein regulates T cell receptor-mediated T cell activation, differentiation and survival. Defects in autoimmunity are restricted to the immune system and not the central nervous system. Our data identify cellular prion protein as a regulator of cellular immunological homoeostasis and suggest cellular prion protein as a novel potential target for therapeutic immunomodulation."],["dc.identifier.doi","10.1093/brain/awp298"],["dc.identifier.isi","000274777700007"],["dc.identifier.pmid","20145049"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20597"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Pharmacological prion protein silencing accelerates central nervous system autoimmune disease via T cell receptor signalling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Bittner, A."],["dc.contributor.author","Jaeger, W."],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Oertel, Wolfgang Hermann"],["dc.contributor.author","Sommer, N."],["dc.contributor.author","Moeller, J. C."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, S."],["dc.date.accessioned","2018-11-07T11:24:24Z"],["dc.date.available","2018-11-07T11:24:24Z"],["dc.date.issued","2009"],["dc.format.extent","436"],["dc.identifier.isi","000268421800026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56397"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","54th Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Increased axonal damage in p75(NTR)-knockout mice after induction of experimental autoimmune encephalomyelitis by adoptive transfer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1269"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Nuclear Medicine"],["dc.bibliographiccitation.lastpage","1276"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Buck, Dorothea"],["dc.contributor.author","Foerschler, Annette"],["dc.contributor.author","Lapa, Constantin"],["dc.contributor.author","Schuster, Tibor"],["dc.contributor.author","Vollmar, Patrick"],["dc.contributor.author","Korn, Thomas"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Drzezga, Alexander"],["dc.contributor.author","Buck, Andreas K."],["dc.contributor.author","Wester, Hans-Juergen"],["dc.contributor.author","Zimmer, Claus"],["dc.contributor.author","Krause, Bernd-Joachim"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T09:07:46Z"],["dc.date.available","2018-11-07T09:07:46Z"],["dc.date.issued","2012"],["dc.description.abstract","Multiple sclerosis (MS) is a heterogeneous disease with respect to lesion pathology, course of disease, and treatment response. Imaging modalities are needed that allow better definition of MS lesions in vivo. The aim of this study was to establish an MRI- and PET/CT-based imaging modality and to evaluate approved and promising PET tracers in experimental autoimmune encephalomyelitis (EAE), the animal model of MS. Methods: MRI and PET/CT scans were obtained in Dark agouti rats with EAE and healthy control rats. The PET tracers 2-F-18-fluoro-2-deoxy-D-glucose (F-18-FDG), 3'-deoxy-3'-F-18-fluorothymidine (F-18-FLT), and O-(2-F-18-fluoro-ethyl)-L-tyrosine (F-18-FET) were used as surrogate markers of glucose utilization, proliferative activity, and amino acid transport and protein biosynthesis. Immediately after the PET/CT scan, animals were sacrificed for autoradiography, histologic work-up, or RNA expression analysis. Results: EAE lesions were predominantly located in the spinal cord. With MRI, we were able to detect inflammatory lesions in diseased rats, which correlated well with inflammatory infiltrates as determined by histology. Increased 18F-FDG uptake was observed in spinal cord lesions in all diseased rats. Further investigation by volume-of-interest analysis demonstrated a correlation between the density of histologically proven cellular infiltrates and the F-18-FDG signal intensity in PET (F-DF=3 = 5.9, P = 0.001) and autoradiography (F-DF=3 = 4.2, P = 0.008). With F-18-FET and F-18-FLT, no definite uptake could be observed on PET scans, whereas autoradiography showed slight radiotracer accumulation in some lesions. Conclusion: Spinal cord inflammatory lesions in the EAE model can be noninvasively visualized in vivo using MRI and F-18-FDG PET/CT. Localized F-18-FDG uptake correlates better with a histologically proven abundance of inflammatory cells as a critical marker of disease activity than MRI. Neither F-18-FET nor F-18-FLT seems to be a suitable marker for the in vivo detection of inflammatory lesions."],["dc.description.sponsorship","German Research Foundation [He2386/7-1, KO 2964/3-1]"],["dc.identifier.doi","10.2967/jnumed.111.102608"],["dc.identifier.isi","000307201300029"],["dc.identifier.pmid","22738927"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25875"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Nuclear Medicine Inc"],["dc.relation.issn","0161-5505"],["dc.title","F-18-FDG PET Detects Inflammatory Infiltrates in Spinal Cord Experimental Autoimmune Encephalomyelitis Lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","264"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","265"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Stueve, Olaf"],["dc.contributor.author","Wang, J."],["dc.contributor.author","Chan, Andrew"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Cepok, Sabine"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Goldman, Myla D."],["dc.contributor.author","Meuth, Sven G."],["dc.contributor.author","Korth, Carsten"],["dc.contributor.author","Lambracht-Washington, Doris"],["dc.date.accessioned","2018-11-07T08:59:22Z"],["dc.date.available","2018-11-07T08:59:22Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1001/archneurol.2010.354"],["dc.identifier.isi","000287330300018"],["dc.identifier.pmid","21320996"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23874"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","No Association Between Genetic Polymorphism at Codon 129 of the Prion Protein Gene and Primary Progressive Multiple Sclerosis"],["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"]]