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","919"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","927"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:06:56Z"],["dc.date.available","2018-11-07T11:06:56Z"],["dc.date.issued","2007"],["dc.description.abstract","To evaluate variations in amyloid beta (A beta) peptide pattern in cerebrospinal fluid (CSF) in neurodegenerative disorders. A recently estabfished quantitative urea-based A beta-sodium-dodecylsulfate-polyacrylamide-gel-electrophoresis with western immunoblot (AP-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide (A beta 1-37, 1-38, 1-39, 1-40, 1-42) pattern in CSF. We asked whether the variation might be useful to further elucidate the overlap between or distinctions among neurodegenerative diseases in A beta-processing. We used the A beta-SDS-PAGE/immunoblot to investigate CSF for diseasespecific A beta peptide patterns. CSF samples from 96 patients with mainly clinically diagnosed Alzheimer's disease (n = 15), progressive supranuclear palsy (n = 20), corticobasal degeneration (n =: 12), Parkinson's disease (n = 11), multiple systems atrophy (n = 18), and dementia with Lewy-bodies (n = 20) were analysed as well a comparison group (n = 19). The A beta peptide patterns varied between tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and a-synuctein on Ap-processing."],["dc.identifier.doi","10.1007/s00702-007-0629-4"],["dc.identifier.isi","000248001800007"],["dc.identifier.pmid","17318305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52433"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Tauopathies and synucleinopathies: Do cerebrospinal fluid beta-amyloid peptides reflect disease-specific pathogenesis?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","396"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","405"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Luk, Connie"],["dc.contributor.author","Compta, Yaroslau"],["dc.contributor.author","Magdalinou, Nadia"],["dc.contributor.author","Jose Marti, Maria"],["dc.contributor.author","Hondhamuni, Geshanthi"],["dc.contributor.author","Zetterberg, Henrik"],["dc.contributor.author","Blennow, Kaj"],["dc.contributor.author","Constantinescu, Radu"],["dc.contributor.author","Pijnenburg, Yolande"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","van Swieten, John"],["dc.contributor.author","Chiu, Wan Zheng"],["dc.contributor.author","Borroni, Barbara"],["dc.contributor.author","Camara, Ana"],["dc.contributor.author","Cheshire, Perdita"],["dc.contributor.author","Williams, David R."],["dc.contributor.author","Lees, Andrew J."],["dc.contributor.author","de Silva, Rohan"],["dc.date.accessioned","2018-11-07T09:04:11Z"],["dc.date.available","2018-11-07T09:04:11Z"],["dc.date.issued","2012"],["dc.description.abstract","Characteristic tau isoform composition of the insoluble fibrillar tau inclusions define tauopathies, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP) and frontotemporal dementia with parkinsonism linked to chromosome 17/frontotemporal lobar degeneration-tau (FTDP-17/FTLD-tau). Exon 10 splicing mutations in the tau gene, MAPT, in familial FTDP-17 cause elevation of tau isoforms with four microtubule-binding repeat domains (4R-tau) compared to those with three repeats (3R-tau). On the basis of two well-characterised monoclonal antibodies against 3R- and 4R-tau, we developed novel, sensitive immuno-PCR assays for measuring the trace amounts of these isoforms in CSF. This was with the aim of assessing if CSF tau isoform changes reflect the pathological changes in tau isoform homeostasis in the degenerative brain and if these would be relevant for differential clinical diagnosis. Initial analysis of clinical CSF samples of PSP (n = 46), corticobasal syndrome (CBS; n = 22), AD (n = 11), Parkinson's disease with dementia (PDD; n = 16) and 35 controls revealed selective decreases of immunoreactive 4R-tau in CSF of PSP and AD patients compared with controls, and lower 4R-tau levels in AD compared with PDD. These decreases could be related to the disease-specific conformational masking of the RD4-binding epitope because of abnormal folding and/or aggregation of the 4R-tau isoforms in tauopathies or increased sequestration of the 4R-tau isoforms in brain tau pathology."],["dc.identifier.doi","10.1111/j.1471-4159.2012.07911.x"],["dc.identifier.isi","000309743600008"],["dc.identifier.pmid","22862741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25061"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3042"],["dc.title","Development and assessment of sensitive immuno-PCR assays for the quantification of cerebrospinal fluid three- and four-repeat tau isoforms in tauopathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Brechlin, Peter"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:33:04Z"],["dc.date.available","2018-11-07T10:33:04Z"],["dc.date.issued","2006"],["dc.description.abstract","Measurement of tau-protein and beta-amyloid(1-42) (A beta 42) in cerebrospinal fluid (CSF) has gained increasing acceptance in the differential diagnosis of Alzheimer's disease. We investigated CSF tau-protein and A beta 42 concentrations in 73 patients with advanced idiopathic Parkinson's disease with dementia (PDD) and 23 patients with idiopathic Parkinson's disease without dementia (PD) and in a comparison group of 41 non-demented neurological patients (CG) using commercially available enzyme-linked-immunoabsorbant- assay ( ELISA). tau-Protein levels were statistically significantly higher and A beta 42 lower in the PDD patients compared to PD patients and the CG. This observation was most marked ( p < 0.05) in a subgroup of patients with PDD carrying the apolipoprotein genotype epsilon 3/epsilon 3. The distribution of the apolipoprotein genotypes in PDD and PD patients was similar to that of the CG. Although a significant difference in tau-protein values was observed between PDD and CG, no diagnostic cut-off value was established. These findings suggest that such protein CSF changes may help to support the clinical diagnosis of cognitive decline in PD and that there may be apolipoprotein-E-isoform- specific differences in CSF protein regulation in advanced PDD. Copyright (C) 2006 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000094871"],["dc.identifier.isi","000242167100003"],["dc.identifier.pmid","16899997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.title","Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","98"],["dc.bibliographiccitation.journal","Parkinsonism & Related Disorders"],["dc.bibliographiccitation.lastpage","101"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Ouled Amar Bencheikh, Bouchra"],["dc.contributor.author","Ruskey, Jennifer A."],["dc.contributor.author","Arnulf, Isabelle"],["dc.contributor.author","Dauvilliers, Yves"],["dc.contributor.author","Monaca, Christelle Charley"],["dc.contributor.author","De Cock, Valérie Cochen"],["dc.contributor.author","Gagnon, Jean-François"],["dc.contributor.author","Spiegelman, Dan"],["dc.contributor.author","Hu, Michele T.M."],["dc.contributor.author","Högl, Birgit"],["dc.contributor.author","Stefani, Ambra"],["dc.contributor.author","Ferini-Strambi, Luigi"],["dc.contributor.author","Plazzi, Giuseppe"],["dc.contributor.author","Antelmi, Elena"],["dc.contributor.author","Young, Peter"],["dc.contributor.author","Heidbreder, Anna"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Oertel, Wolfgang"],["dc.contributor.author","Montplaisir, Jacques Y."],["dc.contributor.author","Postuma, Ronald B."],["dc.contributor.author","Rouleau, Guy A."],["dc.contributor.author","Gan-Or, Ziv"],["dc.date.accessioned","2020-12-10T15:20:41Z"],["dc.date.available","2020-12-10T15:20:41Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.parkreldis.2018.03.019"],["dc.identifier.issn","1353-8020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72760"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","LRRK2 protective haplotype and full sequencing study in REM sleep behavior disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","340"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Zeitschrift für Gerontologie und Geriatrie"],["dc.bibliographiccitation.lastpage","346"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Jacobs, Andreas H."],["dc.contributor.author","Emmert, Kirsten"],["dc.contributor.author","Baron, Ralf"],["dc.contributor.author","Bartsch, Thorsten"],["dc.contributor.author","Bauer, Juergen"],["dc.contributor.author","Becker, Clemens"],["dc.contributor.author","Berg, Daniela"],["dc.contributor.author","Bergmann, Philipp"],["dc.contributor.author","Boetzel, Kai"],["dc.contributor.author","Bollheimer, Cornelius"],["dc.contributor.author","Deuschl, Guenther"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Drey, Michael"],["dc.contributor.author","Durwen, Herbert"],["dc.contributor.author","Ebersbach, Georg"],["dc.contributor.author","Elshehabi, Morad"],["dc.contributor.author","Geritz, Johanna"],["dc.contributor.author","Gisinger, Christoph"],["dc.contributor.author","Guennewig, Thomas"],["dc.contributor.author","Hauptmann, Bjoern"],["dc.contributor.author","Heppner, Hans-Juergen"],["dc.contributor.author","Hobert, Markus A."],["dc.contributor.author","Hofmann, Werner"],["dc.contributor.author","Huellemann, Philipp"],["dc.contributor.author","Jahn, Klaus"],["dc.contributor.author","Klucken, Jochen"],["dc.contributor.author","Kurth, Roland"],["dc.contributor.author","Lindner, Reinhard"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Lukas, Albert"],["dc.contributor.author","Maetzold, Sara"],["dc.contributor.author","Mokrusch, Thomas"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Plate, Annika"],["dc.contributor.author","Polidori, Maria Cristina"],["dc.contributor.author","Prell, Tino"],["dc.contributor.author","Schellinger, Peter"],["dc.contributor.author","Spira, Dominik"],["dc.contributor.author","Stephani, Ulrich"],["dc.contributor.author","Studt, Simone"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Unger, Heinz L."],["dc.contributor.author","Urban, Peter"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Warnecke, Tobias"],["dc.contributor.author","Weiss, Michael"],["dc.contributor.author","Wiedemann, Andreas"],["dc.contributor.author","Wirth, Rainer"],["dc.contributor.author","Witt, Karsten"],["dc.contributor.author","Dodel, Richard"],["dc.contributor.author","Maetzler, Walter"],["dc.date.accessioned","2020-12-10T14:10:21Z"],["dc.date.available","2020-12-10T14:10:21Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00391-020-01734-1"],["dc.identifier.eissn","1435-1269"],["dc.identifier.issn","0948-6704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70733"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neurogeriatrie – eine Vision für die verbesserte Versorgung und Forschung für geriatrische Patienten mit führend neurologischen Erkrankungen"],["dc.title.alternative","Neurogeriatrics—a vision for improved care and research for geriatric patients with predominating neurological disabilities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","538"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","540"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Hopfner, Franziska"],["dc.contributor.author","Schulte, Eva C."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bereznai, Benjamin"],["dc.contributor.author","Knauf, Franziska"],["dc.contributor.author","Lichtner, Peter"],["dc.contributor.author","Zimprich, Alexander"],["dc.contributor.author","Haubenberger, Dietrich"],["dc.contributor.author","Pirker, Walter"],["dc.contributor.author","Bruecke, Thomas"],["dc.contributor.author","Peters, Annette"],["dc.contributor.author","Gieger, Christian"],["dc.contributor.author","Kuhlenbaeumer, Gregor"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Winkelmann, Juliane"],["dc.date.accessioned","2018-11-07T09:26:33Z"],["dc.date.available","2018-11-07T09:26:33Z"],["dc.date.issued","2013"],["dc.description.abstract","Background Genetic variation in the glucocerebrosidase (GBA) gene is strongly associated with Parkinson's disease (PD). Transport of glucocerebrosidase to the lysosome involves the protein encoded by the SCARB2 gene. An association between the common SNP rs6812193, upstream of SCARB2, and PD has been reported previously. The role of exonic variants in the SCARB2 gene in PD has not been examined. Methods We studied the role of exonic variants in SCARB2 and tried to replicate the association between the SNP rs6812193 and PD in a German and Austrian sample. Screening of all SCARB2 exons by high-resolution melting curve analysis was performed in 376 German PD patients. The SNP rs6812193 was analyzed in 984 PD patients and 1014 general population controls. Results We identified no novel exonic variants in SCARB2 but confirmed the association between SNP rs6812193 and PD (OR, 0.86; P=.02). (c) 2013 Movement Disorder Society"],["dc.identifier.doi","10.1002/mds.25349"],["dc.identifier.isi","000317366100026"],["dc.identifier.pmid","23408458"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0885-3185"],["dc.title","The role of SCARB2 as susceptibility factor in Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","431"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","SLEEP"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Sixel-Doering, Friederike"],["dc.contributor.author","Trautmann, Ellen"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.date.accessioned","2018-11-07T09:43:16Z"],["dc.date.available","2018-11-07T09:43:16Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective: To analyze potential markers in sleep for early recognition of neurodegenerative disease in newly diagnosed, unmedicated patients with Parkinson disease (PD) compared to controls. Methods: Videopolysomnography (vPSG) was available in 158 newly diagnosed, unmedicated patients with PD and 110 age-, sex-, and education-matched healthy controls (HC). Rapid eye movement (REM) sleep was analyzed for REM without atonia (RWA) and studied by review of time-synchronized video. Motor behaviors and/or vocalizations in REM sleep with a purposeful component other than comfort moves were identified as REM sleep behavioral events (RBE). Two or more events had to be present to be classified as \"RBE positive.\" RBE subjects included rapid eye movement sleep behavior disorder (RBD) and non-RBD subjects based on the presence or absence of RWA > 18.2%. Results: RBE were detected in 81 of 158 patients with de novo PD (51%) and 17 of 110 HC (15%) (P < 0.001). RBD was identified in 40/81 RBE-positive patients with PD (25% of all PD patients) and 2 of 17 RBE-positive HC (2% of all controls). RBE-positive patients showed no specific motor or neuropsychological features compared to RBE-negative patients. Patients with PD and HC with RBE had more REM sleep (P = 0.002) and a higher periodic leg movements in sleep index (P = 0.022) compared to subjects without RBE. Conclusion: This first description of REM sleep behavioral events (RBE) shows it occurs more frequently in patients with de novo Parkinson disease (PD) than in healthy controls and may be an early sign of neurodegeneration and precede rapid eye movement sleep behavior disorder (RBD). There is no specific phenotype of PD associated with newly defined RBE or RBD at this early stage."],["dc.identifier.doi","10.5665/sleep.3468"],["dc.identifier.isi","000332520400001"],["dc.identifier.pmid","24587564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34142"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Acad Sleep Medicine"],["dc.relation.issn","1550-9109"],["dc.relation.issn","0161-8105"],["dc.title","Rapid Eye Movement Sleep Behavioral Events: A New Marker for Neurodegeneration in Early Parkinson Disease?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","142.e5"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","142.e7"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Rudakou, Uladzislau"],["dc.contributor.author","Futhey, Naomi C."],["dc.contributor.author","Krohn, Lynne"],["dc.contributor.author","Ruskey, Jennifer A."],["dc.contributor.author","Heilbron, Karl"],["dc.contributor.author","Cannon, Paul"],["dc.contributor.author","Alam, Armaghan"],["dc.contributor.author","Arnulf, Isabelle"],["dc.contributor.author","Hu, Michele T.M."],["dc.contributor.author","Montplaisir, Jacques Y."],["dc.contributor.author","Gagnon, Jean-François"],["dc.contributor.author","Desautels, Alex"],["dc.contributor.author","Dauvilliers, Yves"],["dc.contributor.author","Toffoli, Marco"],["dc.contributor.author","Gigli, Gian Luigi"],["dc.contributor.author","Valente, Mariarosaria"],["dc.contributor.author","Högl, Birgit"],["dc.contributor.author","Stefani, Ambra"],["dc.contributor.author","Holzknecht, Evi"],["dc.contributor.author","Sonka, Karel"],["dc.contributor.author","Kemlink, David"],["dc.contributor.author","Oertel, Wolfang"],["dc.contributor.author","Janzen, Annette"],["dc.contributor.author","Plazzi, Giuseppe"],["dc.contributor.author","Antelmi, Elena"],["dc.contributor.author","Figorilli, Michela"],["dc.contributor.author","Puligheddu, Monica"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","De Cock, Valérie Cochen"],["dc.contributor.author","Monaca, Christelle Charley"],["dc.contributor.author","Heidbreder, Anna"],["dc.contributor.author","Ferini-Strambi, Luigi"],["dc.contributor.author","Dijkstra, Femke"],["dc.contributor.author","Viaene, Mineke"],["dc.contributor.author","Abril, Beatriz"],["dc.contributor.author","Boeve, Bradley F."],["dc.contributor.author","Postuma, Ronald B."],["dc.contributor.author","Rouleau, Guy A."],["dc.contributor.author","Gan-Or, Ziv"],["dc.date.accessioned","2021-04-14T08:23:22Z"],["dc.date.available","2021-04-14T08:23:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.neurobiolaging.2020.04.005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80887"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0197-4580"],["dc.title","SMPD1 variants do not have a major role in rapid eye movement sleep behavior disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]