Mollenhauer, Brit

[["dc.bibliographiccitation.firstpage","739"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","746"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trautmann, Ellen"],["dc.contributor.author","Otte, Birgit"],["dc.contributor.author","Ng, Juliana"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Sixel-Doering, Friederike"],["dc.contributor.author","Hakimi, Mansoureh"],["dc.contributor.author","VonSattel, Jean-Paul"],["dc.contributor.author","Nussbaum, Robert"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Schlossmacher, Michael G."],["dc.date.accessioned","2018-11-07T09:08:50Z"],["dc.date.available","2018-11-07T09:08:50Z"],["dc.date.issued","2012"],["dc.description.abstract","The source of Parkinson disease-linked alpha-synuclein (aSyn) in human cerebrospinal fluid (CSF) remains unknown. We decided to measure the concentration of aSyn and its gradient in human CSF specimens and compared it with serum to explore its origin. We correlated aSyn concentrations in CSF versus serum (Q(aSyn)) to the albumin quotient (Q(albumin)) to evaluate its relation to blood-CSF barrier function. We also compared aSyn with several other CSF constituents of either central or peripheral sources (or both) including albumin, neuron-specific enolase, beta-trace protein and total protein content. Finally, we examined whether aSyn is present within the structures of the choroid plexus (CP). We observed that Q(aSyn) did not rise or fall with Q(albumin) values, a relative measure of blood-CSF barrier integrity. In our CSF gradient analyses, aSyn levels decreased slightly from rostral to caudal fractions, in parallel to the recorded changes for neuron-specific enolase; the opposite trend was recorded for total protein, albumin and beta-trace protein. The latter showed higher concentrations in caudal CSF fractions due to the diffusion-mediated transfer of proteins from blood and leptomeninges into CSF in the lower regions of the spine. In postmortem sections of human brain, we detected highly variable aSyn reactivity within the epithelial cell layer of CP in patients diagnosed with a range of neurological diseases; however, in sections of mice that express only human SNCA alleles (and in those without any Snca gene expression), we detected no aSyn signal in the epithelial cells of the CP. We conclude from these complementary results that despite its higher levels in peripheral blood products, neurons of the brain and spinal cord represent the principal source of aSyn in human CSF."],["dc.identifier.doi","10.1007/s00702-012-0784-0"],["dc.identifier.isi","000305525800002"],["dc.identifier.pmid","22426833"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26122"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","alpha-Synuclein in human cerebrospinal fluid is principally derived from neurons of the central nervous system"],["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","856"],["dc.bibliographiccitation.issue","6518"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","860"],["dc.bibliographiccitation.volume","370"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Ojha, Ravi"],["dc.contributor.author","Pedro, Liliana D."],["dc.contributor.author","Djannatian, Minou"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Kuivanen, Suvi"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Kallio, Katri"],["dc.contributor.author","Kaya, Tuğberk"],["dc.contributor.author","Anastasina, Maria"],["dc.contributor.author","Smura, Teemu"],["dc.contributor.author","Levanov, Lev"],["dc.contributor.author","Szirovicza, Leonora"],["dc.contributor.author","Tobi, Allan"],["dc.contributor.author","Kallio-Kokko, Hannimari"],["dc.contributor.author","Österlund, Pamela"],["dc.contributor.author","Joensuu, Merja"],["dc.contributor.author","Meunier, Frédéric A."],["dc.contributor.author","Butcher, Sarah J."],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Helenius, Ari"],["dc.contributor.author","Gokce, Ozgun"],["dc.contributor.author","Teesalu, Tambet"],["dc.contributor.author","Hepojoki, Jussi"],["dc.contributor.author","Vapalahti, Olli"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Balistreri, Giuseppe"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2021-04-14T08:31:26Z"],["dc.date.available","2021-04-14T08:31:26Z"],["dc.date.issued","2020"],["dc.description.abstract","The causative agent of coronavirus disease 2019 (COVID-19) is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). For many viruses, tissue tropism is determined by the availability of virus receptors and entry cofactors on the surface of host cells. In this study, we found that neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, an effect blocked by a monoclonal blocking antibody against NRP1. A SARS-CoV-2 mutant with an altered furin cleavage site did not depend on NRP1 for infectivity. Pathological analysis of olfactory epithelium obtained from human COVID-19 autopsies revealed that SARS-CoV-2 infected NRP1-positive cells facing the nasal cavity. Our data provide insight into SARS-CoV-2 cell infectivity and define a potential target for antiviral intervention."],["dc.identifier.doi","10.1126/science.abd2985"],["dc.identifier.pmid","33082293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83594"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/73"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/8"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A06: The role of lipid-sensing nuclear receptors as checkpoints in regulating phagocyte function during recovery from demyelinating injury"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Cantuti"],["dc.relation.workinggroup","RG Gokce (Systems Neuroscience – Cell Diversity)"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.rights","CC BY 4.0"],["dc.title","Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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.artnumber","121"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.affiliation","Lerche, Stefanie;"],["dc.contributor.affiliation","Heinzel, Sebastian;"],["dc.contributor.affiliation","Alves, Guido W.;"],["dc.contributor.affiliation","Barone, Paolo;"],["dc.contributor.affiliation","Behnke, Stefanie;"],["dc.contributor.affiliation","Ben-Shlomo, Yoav;"],["dc.contributor.affiliation","Berendse, Henk;"],["dc.contributor.affiliation","Bloem, Bastiaan R.;"],["dc.contributor.affiliation","Burn, David;"],["dc.contributor.affiliation","Dodel, Richard;"],["dc.contributor.affiliation","Grosset, Donald G.;"],["dc.contributor.affiliation","Hipp, Geraldine;"],["dc.contributor.affiliation","Hu, Michele T.;"],["dc.contributor.affiliation","Kasten, Meike;"],["dc.contributor.affiliation","Krüger, Rejko;"],["dc.contributor.affiliation","Liepelt-Scarfone, Inga;"],["dc.contributor.affiliation","Maetzler, Walter;"],["dc.contributor.affiliation","Moccia, Marcello;"],["dc.contributor.affiliation","Mollenhauer, Brit;"],["dc.contributor.affiliation","Oertel, Wolfgang;"],["dc.contributor.affiliation","Roeben, Benjamin;"],["dc.contributor.affiliation","Walter, Uwe;"],["dc.contributor.affiliation","Wirdefeldt, Karin;"],["dc.contributor.affiliation","Berg, Daniela;"],["dc.contributor.author","Lerche, Stefanie"],["dc.contributor.author","Heinzel, Sebastian"],["dc.contributor.author","Alves, Guido W."],["dc.contributor.author","Barone, Paolo"],["dc.contributor.author","Behnke, Stefanie"],["dc.contributor.author","Ben-Shlomo, Yoav"],["dc.contributor.author","Berendse, Henk W."],["dc.contributor.author","Bloem, Bastiaan R."],["dc.contributor.author","Burns, David J."],["dc.contributor.author","Dodel, Richard"],["dc.contributor.author","Grosset, Donald G."],["dc.contributor.author","Hipp, Geraldine"],["dc.contributor.author","Hu, Michele T. M."],["dc.contributor.author","Kasten, Meike"],["dc.contributor.author","Krüger, Rejko"],["dc.contributor.author","Liepelt-Scarfone, Inga"],["dc.contributor.author","Moccia, Marcello"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Oertel, Wolfgang"],["dc.contributor.author","Roeben, Benjamin"],["dc.contributor.author","Walter, Uwe"],["dc.contributor.author","Wirdefeldt, Karin"],["dc.contributor.author","Maetzler, Walter"],["dc.contributor.author","Berg, Daniela"],["dc.date.accessioned","2018-11-07T10:14:05Z"],["dc.date.available","2018-11-07T10:14:05Z"],["dc.date.issued","2016"],["dc.date.updated","2022-02-09T13:23:10Z"],["dc.identifier.doi","10.3389/fnagi.2016.00121"],["dc.identifier.eissn","1663-4365"],["dc.identifier.isi","000376574700001"],["dc.identifier.pmid","27303289"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13374"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40560"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1663-4365"],["dc.relation.issn","1663-4365"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Aiming for Study Comparability in Parkinson's Disease: Proposal for a Modular Set of Biomarker Assessments to be Used in Longitudinal Studies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","822"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY"],["dc.bibliographiccitation.lastpage","832"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Doss, Sarah"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Hyman, Bradley T."],["dc.contributor.author","Panzer, Jessica A."],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Dickerson, Bradford"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Scherzer, Clemens R."],["dc.contributor.author","Ivinson, Adrian J."],["dc.contributor.author","Finke, Carsten"],["dc.contributor.author","Schoels, Ludger"],["dc.contributor.author","vom Hagen, Jennifer Muller"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Hoeltje, Markus"],["dc.contributor.author","Biswal, Bharat B."],["dc.contributor.author","Harms, Lutz"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Buchert, Ralph"],["dc.contributor.author","Hoeglinger, Guenther U."],["dc.contributor.author","Oertel, Wolfgang Hermann"],["dc.contributor.author","Unger, Marcus Michael"],["dc.contributor.author","Koertvelyessy, Peter"],["dc.contributor.author","Bittner, Daniel"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Spruth, Eike J."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Meisel, Andreas"],["dc.contributor.author","Lynch, David R."],["dc.contributor.author","Dirnagl, Ulrich"],["dc.contributor.author","Endres, Matthias"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Komorowski, Lars"],["dc.contributor.author","Stoecker, Winfried"],["dc.contributor.author","Dalmau, Josep"],["dc.contributor.author","Pruess, Harald"],["dc.date.accessioned","2018-11-07T09:34:55Z"],["dc.date.available","2018-11-07T09:34:55Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective: To retrospectively determine the frequency of N-Methyl-D-Aspartate (NMDA) receptor (NMDAR) autoantibodies in patients with different forms of dementia. Methods: Clinical characterization of 660 patients with dementia, neurodegenerative disease without dementia, other neurological disorders and age-matched healthy controls combined with retrospective analysis of serum or cerebrospinal fluid (CSF) for the presence of NMDAR antibodies. Antibody binding to receptor mutants and the effect of immunotherapy were determined in a subgroup of patients. Results: Serum NMDAR antibodies of IgM, IgA, or IgG subtypes were detected in 16.1% of 286 dementia patients (9.5% IgM, 4.9% IgA, and 1.7% IgG) and in 2.8% of 217 cognitively healthy controls (1.9% IgM and 0.9% IgA). Antibodies were rarely found in CSF. The highest prevalence of serum antibodies was detected in patients with \"unclassified dementia\" followed by progressive supranuclear palsy, corticobasal syndrome, Parkinson's disease-related dementia, and primary progressive aphasia. Among the unclassified dementia group, 60% of 20 patients had NMDAR antibodies, accompanied by higher frequency of CSF abnormalities, and subacute or fluctuating disease progression. Immunotherapy in selected prospective cases resulted in clinical stabilization, loss of antibodies, and improvement of functional imaging parameters. Epitope mapping showed varied determinants in patients with NMDAR IgA-associated cognitive decline. Interpretation: Serum IgA/IgM NMDAR antibodies occur in a significant number of patients with dementia. Whether these antibodies result from or contribute to the neurodegenerative disorder remains unknown, but our findings reveal a subgroup of patients with high antibody levels who can potentially benefit from immunotherapy."],["dc.description.sponsorship","NINDS NIH HHS [U01 NS082157, K12 NS049453, R01 NS077851, U01 NS082080]"],["dc.identifier.doi","10.1002/acn3.120"],["dc.identifier.isi","000209815600008"],["dc.identifier.pmid","25493273"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11774"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32281"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2328-9503"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","High prevalence of NMDA receptor IgA/IgM antibodies in different dementia types"],["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","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","265"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schneider, Michael"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Gross, Martin"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T11:19:48Z"],["dc.date.available","2018-11-07T11:19:48Z"],["dc.date.issued","2008"],["dc.description.abstract","Background/Aims: The study evaluated the patterns of cerebrospinal fluid (CSF), amyloid-beta (A beta) peptides, total tau and phospho-tau among Alzheimer's disease (AD) and vascular dementias (VAD). Methods: A beta-SDS-PAGE immunoblot and commercially available ELISAs were applied to the CSF analysis of 52 patients with probable (n = 21) and possible (n = 16) VAD, AD with cerebrovascular disease (n = 15), 30 patients with probable AD and 30 nondemented disease controls. Results: AD and AD with cerebrovascular disease displayed a similar neurochemical phenotype in contrast to nondemented disease controls and probable VAD with regard to tau, p-tau, A beta-40(ox) and A beta 1-42%. Possible VAD displayed AD-like changes only for A beta 1-40(ox) and A beta 1-42%. Conclusion: CSF neurochemical phenotypes sufficiently discriminate probable AD and VAD from each other, but their diagnostic value is limited in case of no clear-cut clinical appearance, such as possible VAD. Conversely, CSF A beta peptides and p-tau levels may help estimate the involvement of AD-like pathophysiological pathways in VAD subgroups. Copyright (c) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000115975"],["dc.identifier.isi","000253777500009"],["dc.identifier.pmid","18270488"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55373"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid neurochemical phenotypes in vascular dementias: Original data and mini-review"],["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","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.firstpage","461"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring"],["dc.bibliographiccitation.lastpage","470"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Heslegrave, Amanda"],["dc.contributor.author","Gupta, Vandana"],["dc.contributor.author","Foiani, Martha"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Lehmann, Sylvain"],["dc.contributor.author","Teunissen, Charlotte"],["dc.contributor.author","Blennow, Kaj"],["dc.contributor.author","Zetterberg, Henrik"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2019-07-09T11:49:35Z"],["dc.date.available","2019-07-09T11:49:35Z"],["dc.date.issued","2018"],["dc.description.abstract","ntroduction: Cerebrospinal fluid α-synuclein level is increased in sporadic Creutzfeldt-Jakob disease cases. However, the clinical value of this biomarker remains to be established. In this study, we have addressed the clinical validation parameters and the interlaboratory reproducibility by using an electrochemiluminescent assay. Methods: Cerebrospinal fluid α-synuclein was quantified in a total of 188 sporadic Creutzfeldt-Jakob disease and non-Creutzfeldt-Jakob-disease cases to determine sensitivity and specificity values and lot-to-lot variability. Two round robin tests with 70 additional cases were performed in six independent laboratories. Results: A sensitivity of 93% and a specificity of 96% were achieved in discriminating sporadic Creutzfeldt-Jakob disease. No differences were detected between lots. The mean interlaboratory coefficient of variation was 23%, and the intralaboratory coefficient of variations ranged 2.70%-11.39%. Overall, 97% of samples were correctly diagnosed. Discussion: The herein validated α-synuclein assay is robust, accurate, and reproducible in identifying Creutzfeldt-Jakob disease cases. Thus, it is ready for implementation in the clinical practice to support the diagnosis of Creutzfeldt-Jakob disease."],["dc.identifier.doi","10.1016/j.dadm.2018.06.005"],["dc.identifier.pmid","30294658"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59586"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Interlaboratory validation of cerebrospinal fluid α-synuclein quantification in the diagnosis of sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","744"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","759"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Postuma, Ronald B."],["dc.contributor.author","Iranzo, Alex"],["dc.contributor.author","Hu, Michele"],["dc.contributor.author","Högl, Birgit"],["dc.contributor.author","Boeve, Bradley F."],["dc.contributor.author","Manni, Raffaele"],["dc.contributor.author","Oertel, Wolfgang H."],["dc.contributor.author","Arnulf, Isabelle"],["dc.contributor.author","Ferini-Strambi, Luigi"],["dc.contributor.author","Puligheddu, Monica"],["dc.contributor.author","Antelmi, Elena"],["dc.contributor.author","Cochen De Cock, Valerie"],["dc.contributor.author","Arnaldi, Dario"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Videnovic, Aleksandar"],["dc.contributor.author","Sonka, Karel"],["dc.contributor.author","Jung, Ki-Young"],["dc.contributor.author","Kunz, Dieter"],["dc.contributor.author","Dauvilliers, Yves"],["dc.contributor.author","Provini, Federica"],["dc.contributor.author","Lewis, Simon J."],["dc.contributor.author","Buskova, Jitka"],["dc.contributor.author","Pavlova, Milena"],["dc.contributor.author","Heidbreder, Anna"],["dc.contributor.author","Montplaisir, Jacques Y."],["dc.contributor.author","Santamaria, Joan"],["dc.contributor.author","Barber, Thomas R."],["dc.contributor.author","Stefani, Ambra"],["dc.contributor.author","St.Louis, Erik K."],["dc.contributor.author","Terzaghi, Michele"],["dc.contributor.author","Janzen, Annette"],["dc.contributor.author","Leu-Semenescu, Smandra"],["dc.contributor.author","Plazzi, Guiseppe"],["dc.contributor.author","Nobili, Flavio"],["dc.contributor.author","Sixel-Doering, Friederike"],["dc.contributor.author","Dusek, Petr"],["dc.contributor.author","Bes, Frederik"],["dc.contributor.author","Cortelli, Pietro"],["dc.contributor.author","Ehgoetz Martens, Kaylena"],["dc.contributor.author","Gagnon, Jean-Francois"],["dc.contributor.author","Gaig, Carles"],["dc.contributor.author","Zucconi, Marco"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Gan-Or, Ziv"],["dc.contributor.author","Lo, Christine"],["dc.contributor.author","Rolinski, Michal"],["dc.contributor.author","Mahlknecht, Philip"],["dc.contributor.author","Holzknecht, Evi"],["dc.contributor.author","Boeve, Angel R."],["dc.contributor.author","Teigen, Luke N."],["dc.contributor.author","Toscano, Gianpaolo"],["dc.contributor.author","Mayer, Geert"],["dc.contributor.author","Morbelli, Silvia"],["dc.contributor.author","Dawson, Benjamin"],["dc.contributor.author","Pelletier, Amelie"],["dc.date.accessioned","2020-03-04T10:32:28Z"],["dc.date.accessioned","2021-10-27T13:22:09Z"],["dc.date.available","2020-03-04T10:32:28Z"],["dc.date.available","2021-10-27T13:22:09Z"],["dc.date.issued","2019"],["dc.description.abstract","Idiopathic REM sleep behaviour disorder (iRBD) is a powerful early sign of Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. This provides an unprecedented opportunity to directly observe prodromal neurodegenerative states, and potentially intervene with neuroprotective therapy. For future neuroprotective trials, it is essential to accurately estimate phenoconversion rate and identify potential predictors of phenoconversion. This study assessed the neurodegenerative disease risk and predictors of neurodegeneration in a large multicentre cohort of iRBD. We combined prospective follow-up data from 24 centres of the International RBD Study Group. At baseline, patients with polysomnographically-confirmed iRBD without parkinsonism or dementia underwent sleep, motor, cognitive, autonomic and special sensory testing. Patients were then prospectively followed, during which risk of dementia and parkinsonsim were assessed. The risk of dementia and parkinsonism was estimated with Kaplan-Meier analysis. Predictors of phenoconversion were assessed with Cox proportional hazards analysis, adjusting for age, sex, and centre. Sample size estimates for disease-modifying trials were calculated using a time-to-event analysis. Overall, 1280 patients were recruited. The average age was 66.3 ± 8.4 and 82.5% were male. Average follow-up was 4.6 years (range = 1-19 years). The overall conversion rate from iRBD to an overt neurodegenerative syndrome was 6.3% per year, with 73.5% converting after 12-year follow-up. The rate of phenoconversion was significantly increased with abnormal quantitative motor testing [hazard ratio (HR) = 3.16], objective motor examination (HR = 3.03), olfactory deficit (HR = 2.62), mild cognitive impairment (HR = 1.91-2.37), erectile dysfunction (HR = 2.13), motor symptoms (HR = 2.11), an abnormal DAT scan (HR = 1.98), colour vision abnormalities (HR = 1.69), constipation (HR = 1.67), REM atonia loss (HR = 1.54), and age (HR = 1.54). There was no significant predictive value of sex, daytime somnolence, insomnia, restless legs syndrome, sleep apnoea, urinary dysfunction, orthostatic symptoms, depression, anxiety, or hyperechogenicity on substantia nigra ultrasound. Among predictive markers, only cognitive variables were different at baseline between those converting to primary dementia versus parkinsonism. Sample size estimates for definitive neuroprotective trials ranged from 142 to 366 patients per arm. This large multicentre study documents the high phenoconversion rate from iRBD to an overt neurodegenerative syndrome. Our findings provide estimates of the relative predictive value of prodromal markers, which can be used to stratify patients for neuroprotective trials."],["dc.identifier.doi","10.1093/brain/awz030"],["dc.identifier.pmid","30789229"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92072"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Risk and predictors of dementia and parkinsonism in idiopathic REM sleep behaviour disorder: a multicentre study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","684"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","DEUTSCHES ARZTEBLATT INTERNATIONAL"],["dc.bibliographiccitation.lastpage","U31"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Foerstl, Hans"],["dc.contributor.author","Deuschl, Guenther"],["dc.contributor.author","Storch, Alexander"],["dc.contributor.author","Oertel, Wolfgang"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2018-11-07T08:38:20Z"],["dc.date.available","2018-11-07T08:38:20Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are the two most common types of dementing neurodegenerative disease after Alzheimer's disease (AD). Both of these conditions are often diagnosed late or not at all. Methods: Selective literature review. Results: The severe cholinergic and dopaminergic deficits that are present in both DLB and PDD produce not only motor manifestations, but also cognitive deficits, mainly in the executive and visual-constructive areas, as well as psychotic manifestations such as visual hallucinations, delusions, and agitation. The intensity of these manifestations can fluctuate markedly over the course of the day, particularly in DLB. Useful tests for differential diagnosis include magnetic resonance imaging and electroencephalography; in case of clinical uncertainty, nuclear medical procedures and cerebrospinal fluid analysis can be helpful as well. Neuropathological studies have revealed progressive alpha-synuclein aggregation in affected areas of the brain. In DLB, beta-amyloid abnormalities are often seen as well. Conclusion: DLB should be included in the differential diagnosis of early dementia. If motor manifestations arise within one year (DLB), dopaminergic treatment should be initiated. On the other hand, patients with Parkinson's disease should undergo early screening for signs of dementia so that further diagnostic and therapeutic steps can be taken in timely fashion, as indicated. Cholinesterase inhibitors are useful for the treatment of cognitive deficits and experiential/behavioral disturbances in both DLB (off-label indication) and PDD (approved indication)."],["dc.identifier.doi","10.3238/arztebl.2010.0684"],["dc.identifier.isi","000283379500003"],["dc.identifier.pmid","20963199"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18746"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Deutscher Aerzte-verlag Gmbh"],["dc.relation.issn","1866-0452"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Lewy Body and Parkinsonian Dementia Common, but Often Misdiagnosed Conditions"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]