Schulz, Jörg Bernhard

[["dc.bibliographiccitation.artnumber","11"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Neurodegeneration"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Hopfner, Franziska"],["dc.contributor.author","Müller, Stefanie H."],["dc.contributor.author","Steppat, Dagmar"],["dc.contributor.author","Miller, Joanna"],["dc.contributor.author","Schmidt, Nele"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Leypoldt, Frank"],["dc.contributor.author","Berg, Daniela"],["dc.contributor.author","Franke, Andre"],["dc.contributor.author","Lieb, Wolfgang"],["dc.contributor.author","Tittmann, Lukas"],["dc.contributor.author","Balzer-Geldsetzer, Monika"],["dc.contributor.author","Baudrexel, Simon"],["dc.contributor.author","Dodel, Richard"],["dc.contributor.author","Hilker-Roggendorf, Ruediger"],["dc.contributor.author","Kalbe, Elke"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Klockgether, Thomas"],["dc.contributor.author","Liepelt-Scarfone, Inga"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Neuser, Petra"],["dc.contributor.author","Reetz, Kathrin"],["dc.contributor.author","Riedel, Oliver"],["dc.contributor.author","Schulte, Claudia"],["dc.contributor.author","Schulz, Jörg B."],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Storch, Alexander"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wittchen, Hans-Ulrich"],["dc.contributor.author","Witt, Karsten"],["dc.contributor.author","Wüllner, Ullrich"],["dc.contributor.author","Deuschl, Günther"],["dc.contributor.author","Kuhlenbäumer, Gregor"],["dc.date.accessioned","2019-07-09T11:51:41Z"],["dc.date.available","2019-07-09T11:51:41Z"],["dc.date.issued","2019"],["dc.description.abstract","Background: IgG-class autoantibodies to N-Methyl-D-Aspartate (NMDA)-type glutamate receptors define a novel entity of autoimmune encephalitis. Studies examining the prevalence of NMDA IgA/IgM antibodies in patients with Parkinson disease with/without dementia produced conflicting results. We measured NMDA antibodies in a large, well phenotyped sample of Parkinson patients without and with cognitive impairment (n = 296) and controls (n = 295) free of neuropsychiatric disease. Detailed phenotyping and large numbers allowed statistically meaningful correlation of antibody status with diagnostic subgroups as well as quantitative indicators of disease severity and cognitive impairment. Methods: NMDA antibodies were analysed in the serum of patients and controls using well established validated assays. We used anti-NMDA antibody positivity as the main independent variable and correlated it with disease status and phenotypic characteristics. Results: The frequency of NMDA IgA/IgM antibodies was lower in Parkinson patients (13%) than in controls (22%) and higher than in previous studies in both groups. NMDA IgA/IgM antibodies were neither significantly associated with diagnostic subclasses of Parkinson disease according to cognitive impairment, nor with quantitative indicators of disease severity and cognitive impairment. A positive NMDA antibody status was positively correlated with age in controls but not in Parkinson patients. Conclusion: It is unlikely albeit not impossible that NMDA antibodies play a significant role in the pathogenesis or progression of Parkinson disease e.g. to Parkinson disease with dementia, while NMDA IgG antibodies define a separate disease of its own."],["dc.identifier.doi","10.1186/s40035-019-0153-0"],["dc.identifier.pmid","30984390"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16171"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59990"],["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","No association between Parkinson disease and autoantibodies against NMDA-type glutamate receptors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e12247"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Herholz, David"],["dc.contributor.author","Fiesel, Fabienne C."],["dc.contributor.author","Kaur, Kavita"],["dc.contributor.author","Müller, Daniel"],["dc.contributor.author","Karsten, Peter"],["dc.contributor.author","Weber, Stephanie S."],["dc.contributor.author","Kahle, Philipp J."],["dc.contributor.author","Marquardt, Till"],["dc.contributor.author","Schulz, Jörg"],["dc.date.accessioned","2019-07-09T11:53:07Z"],["dc.date.available","2019-07-09T11:53:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Alteration and/or mutations of the ribonucleoprotein TDP-43 have been firmly linked to human neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). The relative impacts of TDP-43 alteration, mutation, or inherent protein function on neural integrity, however, remain less clear--a situation confounded by conflicting reports based on transient and/or random-insertion transgenic expression. We therefore performed a stringent comparative investigation of impacts of these TDP-43 modifications on neural integrity in vivo. To achieve this, we systematically screened ALS/FTLD-associated and synthetic TDP-43 isoforms via same-site gene insertion and neural expression in Drosophila; followed by transposon-based motor neuron-specific transgenesis in a chick vertebrate system. Using this bi-systemic approach we uncovered a requirement of inherent TDP-43 RNA-binding function--but not ALS/FTLD-linked mutation, mislocalization, or truncation--for TDP-43-mediated neurotoxicity in vivo."],["dc.identifier.doi","10.1371/journal.pone.0012247"],["dc.identifier.fs","573853"],["dc.identifier.pmid","20806063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60347"],["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","Amyotrophic Lateral Sclerosis"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Cell Line"],["dc.subject.mesh","Chickens"],["dc.subject.mesh","DNA-Binding Proteins"],["dc.subject.mesh","Drosophila melanogaster"],["dc.subject.mesh","Frontotemporal Lobar Degeneration"],["dc.subject.mesh","Gene Expression Regulation"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Intracellular Space"],["dc.subject.mesh","Locomotion"],["dc.subject.mesh","Longevity"],["dc.subject.mesh","Male"],["dc.subject.mesh","Motor Neurons"],["dc.subject.mesh","Mutation"],["dc.subject.mesh","Neurons"],["dc.subject.mesh","Organ Specificity"],["dc.subject.mesh","Protein Binding"],["dc.subject.mesh","Protein Transport"],["dc.subject.mesh","RNA"],["dc.title","TDP-43-mediated neuron loss in vivo requires RNA-binding activity."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]