Linker, Ralf Andreas

[["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.artnumber","e7624"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Lee, D. H."],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:52:40Z"],["dc.date.available","2019-07-09T11:52:40Z"],["dc.date.issued","2009-10-28"],["dc.description.abstract","The identification of new biomarkers is of high interest for the prediction of the disease course and also for the identification of pathomechanisms in multiple sclerosis (MS). To specify markers of the chronic disease phase, we performed proteome profiling during the later phase of myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis (MOG-EAE, day 35 after immunization) as a model disease mimicking many aspects of secondary progressive MS. In comparison to healthy controls, high resolution 2 dimensional gel electrophoresis revealed a number of regulated proteins, among them glial fibrilary acidic protein (GFAP). Phase specific up-regulation of GFAP in chronic EAE was confirmed by western blotting and immunohistochemistry. Protein levels of GFAP were also increased in the cerebrospinal fluid of MS patients with specificity for the secondary progressive disease phase. In a next step, proteome profiling of an EAE model with enhanced degenerative mechanisms revealed regulation of alpha-internexin, syntaxin binding protein 1, annexin V and glutamate decarboxylase in the ciliary neurotrophic factor (CNTF) knockout mouse. The identification of these proteins implicate an increased apoptosis and enhanced axonal disintegration and correlate well the described pattern of tissue injury in CNTF -/- mice which involve oligodendrocyte (OL) apoptosis and axonal injury.In summary, our findings underscore the value of proteome analyses as screening method for stage specific biomarkers and for the identification of new culprits for tissue damage in chronic autoimmune demyelination."],["dc.format.extent","9"],["dc.identifier.doi","10.1371/journal.pone.0007624"],["dc.identifier.fs","544326"],["dc.identifier.pmid","19865482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5819"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Axons"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Encephalomyelitis, Autoimmune, Experimental"],["dc.subject.mesh","Gene Expression Profiling"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Multiple Sclerosis"],["dc.subject.mesh","Oligodendroglia"],["dc.subject.mesh","Proteome"],["dc.subject.mesh","Proteomics"],["dc.subject.mesh","Time Factors"],["dc.title","Proteome profiling in murine models of multiple sclerosis: identification of stage specific markers and culprits for tissue damage."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e010956"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","BMJ Open"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Molnar, Fanni"],["dc.contributor.author","Beisse, Flemming"],["dc.contributor.author","Gross, Nikolai"],["dc.contributor.author","Drueschler, Katharina"],["dc.contributor.author","Heinrich, Sven P."],["dc.contributor.author","Joachimsen, Lutz"],["dc.contributor.author","Rauer, Sebastian"],["dc.contributor.author","Pielen, Amelie"],["dc.contributor.author","Suehs, Kurt-Wolfram"],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Huchzermeyer, Cord"],["dc.contributor.author","Albrecht, Philipp"],["dc.contributor.author","Hassenstein, Andrea"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Guthoff, Tanja"],["dc.contributor.author","Tonagel, Felix"],["dc.contributor.author","Kernstock, Christoph"],["dc.contributor.author","Hartmann, Kathrin"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","van Oterendorp, Christian"],["dc.contributor.author","Grotejohann, Birgit"],["dc.contributor.author","Ihorst, Gabriele"],["dc.contributor.author","Maurer, Julia"],["dc.contributor.author","Mueller, Matthias"],["dc.contributor.author","Volkmann, Martin"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Platten, Michael"],["dc.contributor.author","Wick, Wolfgang"],["dc.contributor.author","Heesen, Christoph"],["dc.contributor.author","Schiefer, Ulrich"],["dc.contributor.author","Wolf, Sebastian"],["dc.contributor.author","Lagreze, Wolf A."],["dc.date.accessioned","2018-11-07T10:20:35Z"],["dc.date.available","2018-11-07T10:20:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Introduction Optic neuritis leads to degeneration of retinal ganglion cells whose axons form the optic nerve. The standard treatment is a methylprednisolone pulse therapy. This treatment slightly shortens the time of recovery but does not prevent neurodegeneration and persistent visual impairment. In a phase II trial performed in preparation of this study, we have shown that erythropoietin protects global retinal nerve fibre layer thickness (RNFLT-G) in acute optic neuritis; however, the preparatory trial was not powered to show effects on visual function. Methods and analysis Treatment of Optic Neuritis with Erythropoietin (TONE) is a national, randomised, double-blind, placebo-controlled, multicentre trial with two parallel arms. The primary objective is to determine the efficacy of erythropoietin compared to placebo given add-on to methylprednisolone as assessed by measurements of RNFLT-G and low-contrast visual acuity in the affected eye 6months after randomisation. Inclusion criteria are a first episode of optic neuritis with decreased visual acuity to 0.5 (decimal system) and an onset of symptoms within 10days prior to inclusion. The most important exclusion criteria are history of optic neuritis or multiple sclerosis or any ocular disease (affected or non-affected eye), significant hyperopia, myopia or astigmatism, elevated blood pressure, thrombotic events or malignancy. After randomisation, patients either receive 33000 international units human recombinant erythropoietin intravenously for 3 consecutive days or placebo (0.9% saline) administered intravenously. With an estimated power of 80%, the calculated sample size is 100 patients. The trial started in September 2014 with a planned recruitment period of 30months. Ethics and dissemination TONE has been approved by the Central Ethics Commission in Freiburg (194/14) and the German Federal Institute for Drugs and Medical Devices (61-3910-4039831). It complies with the Declaration of Helsinki, local laws and ICH-GCP. Trial registration number NCT01962571."],["dc.identifier.doi","10.1136/bmjopen-2015-010956"],["dc.identifier.isi","000374052300146"],["dc.identifier.pmid","26932144"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41917"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","2044-6055"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Treatment of optic neuritis with erythropoietin (TONE): a randomised, double-blind, placebo-controlled trialstudy protocol"],["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","372"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Peseschkian, Tara; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Peseschkian.Tara@mh-hannover.de"],["dc.contributor.affiliation","Cordts, Isabell; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, isabell.cordts@tum.de"],["dc.contributor.affiliation","Günther, René; \t\t \r\n\t\t Department of Neurology, University Hospital Carl Gustav Carus, 01307 Dresden, Germany, Rene.Guenther@uniklinikum-dresden.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 01307 Dresden, Germany, Rene.Guenther@uniklinikum-dresden.de"],["dc.contributor.affiliation","Stolte, Benjamin; \t\t \r\n\t\t Department of Neurology, University Medicine Essen, 45147 Essen, Germany, benjamin.stolte@uk-essen.de"],["dc.contributor.affiliation","Zeller, Daniel; \t\t \r\n\t\t Department of Neurology, University of Würzburg, 97080 Würzburg, Germany, Zeller_D@ukw.de"],["dc.contributor.affiliation","Schröter, Carsten; \t\t \r\n\t\t Hoher Meißner Clinic, Neurology, 37242 Bad Sooden-Allendorf, Germany, Schroeter@reha-klinik.de"],["dc.contributor.affiliation","Weyen, Ute; \t\t \r\n\t\t Department of Neurology, Ruhr-University Bochum, BG-Kliniken Bergmannsheil, 44789 Bochum, Germany, ute.weyen@bergmannsheil.de"],["dc.contributor.affiliation","Regensburger, Martin; \t\t \r\n\t\t Department of Molecular Neurology, Friedrich-Alexander-University Erlangen-Nürnberg, 91054 Erlangen, Germany, Martin.Regensburger@uk-erlangen.de"],["dc.contributor.affiliation","Wolf, Joachim; \t\t \r\n\t\t Department of Neurology, Diakonissen Hospital Mannheim, 68163 Mannheim, Germany, j.wolf@diako-mannheim.de"],["dc.contributor.affiliation","Schneider, Ilka; \t\t \r\n\t\t Department of Neurology, Martin-Luther University Halle/Saale, 06120 Halle, Germany, Ilka.Schneider@sanktgeorg.de\t\t \r\n\t\t Department of Neurology, Klinikum Sankt Georg, 04129 Leipzig, Germany, Ilka.Schneider@sanktgeorg.de"],["dc.contributor.affiliation","Hermann, Andreas; \t\t \r\n\t\t Translational Neurodegeneration Section “Albrecht-Kossel”, Department of Neurology, University Medical Center Rostock, University of Rostock, 18147 Rostock, Germany, Andreas.Hermann@med.uni-rostock.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases Rostock/Greifswald, 18147 Rostock, Germany, Andreas.Hermann@med.uni-rostock.de"],["dc.contributor.affiliation","Metelmann, Moritz; \t\t \r\n\t\t Department of Neurology, University Hospital Leipzig, 04103 Leipzig, Germany, Moritz.Metelmann@medizin.uni-leipzig.de"],["dc.contributor.affiliation","Kohl, Zacharias; \t\t \r\n\t\t Department of Neurology, University of Regensburg, 93053 Regensburg, Germany, zacharias.kohl@klinik.uni-regensburg.de"],["dc.contributor.affiliation","Linker, Ralf A.; \t\t \r\n\t\t Department of Neurology, University of Regensburg, 93053 Regensburg, Germany, Ralf.Linker@klinik.uni-regensburg.de"],["dc.contributor.affiliation","Koch, Jan Christoph; \t\t \r\n\t\t Department of Neurology, University Medicine Göttingen, 37075 Göttingen, Germany, jkoch@med.uni-goettingen.de"],["dc.contributor.affiliation","Büchner, Boriana; \t\t \r\n\t\t Friedrich-Baur Institute, Department of Neurology, University Hospital, Ludwig Maximilian University of Munich, 80336 Munich, Germany, Boriana.Buechner@med.uni-muenchen.de"],["dc.contributor.affiliation","Weiland, Ulrike; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, Ulrike.Weiland@uniklinik-ulm.de"],["dc.contributor.affiliation","Schönfelder, Erik; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Erik.Schoenfelder@stud.mh-hannover.de"],["dc.contributor.affiliation","Heinrich, Felix; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Felix.Heinrich@stud.mh-hannover.de"],["dc.contributor.affiliation","Osmanovic, Alma; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, dr.almaosmanovic@gmail.com"],["dc.contributor.affiliation","Klopstock, Thomas; \t\t \r\n\t\t Friedrich-Baur Institute, Department of Neurology, University Hospital, Ludwig Maximilian University of Munich, 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de\t\t \r\n\t\t Munich Cluster for Systems Neurology (SyNergy), 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de"],["dc.contributor.affiliation","Dorst, Johannes; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, johannes.dorst@rku.de"],["dc.contributor.affiliation","Ludolph, Albert C.; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, albert.ludolph@rku.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 89081 Ulm, Germany, albert.ludolph@rku.de"],["dc.contributor.affiliation","Boentert, Matthias; \t\t \r\n\t\t Department of Neurology with the Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany, Matthias.Boentert@ukmuenster.de\t\t \r\n\t\t Department of Medicine, UKM Marienhospital, 48565 Steinfurt, Germany, Matthias.Boentert@ukmuenster.de"],["dc.contributor.affiliation","Hagenacker, Tim; \t\t \r\n\t\t Department of Neurology, University Medicine Essen, 45147 Essen, Germany, tim.hagenacker@uk-essen.de"],["dc.contributor.affiliation","Deschauer, Marcus; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, marcus.deschauer@mri.tum.de"],["dc.contributor.affiliation","Lingor, Paul; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, paul.lingor@tum.de"],["dc.contributor.affiliation","Petri, Susanne; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Petri.Susanne@mh-hannover.de"],["dc.contributor.affiliation","Schreiber-Katz, Olivia; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Schreiber-Katz.Olivia@mh-hannover.de"],["dc.contributor.author","Peseschkian, Tara"],["dc.contributor.author","Cordts, Isabell"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Stolte, Benjamin"],["dc.contributor.author","Zeller, Daniel"],["dc.contributor.author","Schröter, Carsten"],["dc.contributor.author","Weyen, Ute"],["dc.contributor.author","Regensburger, Martin"],["dc.contributor.author","Wolf, Joachim"],["dc.contributor.author","Schneider, Ilka"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Metelmann, Moritz"],["dc.contributor.author","Kohl, Zacharias"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Büchner, Boriana"],["dc.contributor.author","Weiland, Ulrike"],["dc.contributor.author","Schönfelder, Erik"],["dc.contributor.author","Heinrich, Felix"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Dorst, Johannes"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Boentert, Matthias"],["dc.contributor.author","Hagenacker, Tim"],["dc.contributor.author","Deschauer, Marcus"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Schreiber-Katz, Olivia"],["dc.date.accessioned","2021-04-14T08:27:57Z"],["dc.date.available","2021-04-14T08:27:57Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:21:17Z"],["dc.description.sponsorship","German Neuromuscular Society “Deutsche Gesellschaft fuer Muskelkranke\" e.V."],["dc.identifier.doi","10.3390/brainsci11030372"],["dc.identifier.eissn","2076-3425"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82457"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2076-3425"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","A Nation-Wide, Multi-Center Study on the Quality of Life of ALS Patients in Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.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.artnumber","14"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Geis, Christian"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Kleinschnitz, Christoph"],["dc.contributor.author","Berthele, Achim"],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Hellwig, Kerstin"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Mayer, Christoph A."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Melms, Arthur"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Marziniak, Martin"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Faiss, Juergen H."],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Ettrich, Barbara"],["dc.contributor.author","Zentner, Christian"],["dc.contributor.author","Guthke, Kersten"],["dc.contributor.author","Hofstadt-van Oy, Ulrich"],["dc.contributor.author","Reuss, Reinhard"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Ziemann, Ulf"],["dc.contributor.author","Kern, Peter"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Bergh, Florian Then"],["dc.contributor.author","Boettcher, Tobias"],["dc.contributor.author","Langel, Stefan"],["dc.contributor.author","Liebetrau, Martin"],["dc.contributor.author","Rommer, Paulus S."],["dc.contributor.author","Niehaus, Sabine"],["dc.contributor.author","Muench, Christoph"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl U, Uwe K."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Veauthier, Christian"],["dc.contributor.author","Sieb, Joern P."],["dc.contributor.author","Wilke, Christian"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Paul, Friedemann"],["dc.date.accessioned","2018-11-07T09:14:18Z"],["dc.date.available","2018-11-07T09:14:18Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective: To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods: Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results: Seropositive patients were found to be predominantly female (p < 0.0003), to more often have signs of co-existing autoimmunity (p < 0.00001), and to experience more severe clinical attacks. A visual acuity of <= 0.1 during acute optic neuritis (ON) attacks was more frequent among seropositives (p < 0.002). Similarly, motor symptoms were more common in seropositive patients, the median Medical Research Council scale (MRC) grade worse, and MRC grades <= 2 more frequent, in particular if patients met the 2006 revised criteria (p < 0.005, p < 0.006 and p < 0.01, respectively), the total spinal cord lesion load was higher (p < 0.006), and lesions >= 6 vertebral segments as well as entire spinal cord involvement more frequent (p < 0.003 and p < 0.043). By contrast, bilateral ON at onset was more common in seronegatives (p < 0.007), as was simultaneous ON and myelitis (p < 0.001); accordingly, the time to diagnosis of NMO was shorter in the seronegative group (p < 0.029). The course of disease was more often monophasic in seronegatives (p < 0.008). Seropositives and seronegatives did not differ significantly with regard to age at onset, time to relapse, annualized relapse rates, outcome from relapse (complete, partial, no recovery), annualized EDSS increase, mortality rate, supratentorial brain lesions, brainstem lesions, history of carcinoma, frequency of preceding infections, oligoclonal bands, or CSF pleocytosis. Both the time to relapse and the time to diagnosis was longer if the disease started with ON (p < 0.002 and p < 0.013). Motor symptoms or tetraparesis at first myelitis and > 1 myelitis attacks in the first year were identified as possible predictors of a worse outcome."],["dc.identifier.doi","10.1186/1742-2094-9-14"],["dc.identifier.isi","000300949700001"],["dc.identifier.pmid","22260418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27377"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients"],["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"]]