Mollenhauer, Brit

[["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","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","1"],["dc.bibliographiccitation.journal","Movement Disorders Clinical Practice"],["dc.bibliographiccitation.lastpage","4"],["dc.bibliographiccitation.volume","Early View Status"],["dc.contributor.author","Halsband, Claire"],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Sixel-Döring, Friederike"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2019-07-09T11:45:02Z"],["dc.date.available","2019-07-09T11:45:02Z"],["dc.date.issued","2018"],["dc.description.abstract","Background: Rapid eye movement (REM) sleep behavior disorder (RBD) is one of the most specific prodromal indicators for Parkinson's disease (PD). Objectives: To test the validity of the RBD-Screening Questionnaire (RBDSQ) in assessing RBD in early PD. Methods: The RBDSQ was completed before video-supported polysomnography (vPSG) by 134 de novo PD patients, 109 matched controls without neurological disorder (CTR) and 30 subjects with idiopathic RBD (iRBD) without clinical signs of PD; results were compared with vPSG-confirmed RBD diagnosis. Results and Conclusions: Sensitivity/specificity of the RBDSQ for the PD cohort were 0.44/0.84 at the previously published cut-off score of 6 for PD patients, and the area under the curve (AUC) 0.68 (95% CI, 0.56–0.79). By contrast, in the iRBD/CTR cohort the RBDSQ (cut-off = 5) had a sensitivity/specificity of 0.97/0.84 and an AUC of 0.95 (95% CI, 0.90–1.00). Subanalysis of question 6 only (4 subitems asking for dream enactment) at a cut-off score of 1 revealed a sensitivity of 0.74 and a specificity of 0.70 for the de novo PD cohort, AUC was 0.74 (95% CI, 0.63–0.84). RBDSQ is an insufficient screening tool for RBD in de novo PD. New screening tools for RBD assessment need to be developed."],["dc.identifier.doi","10.1002/mdc3.12591"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15012"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59145"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/634821/EU//PROPAG-AGEING"],["dc.relation.issn","2330-1619"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The REM Sleep Behavior Disorder Screening Questionnaire is not Valid in De Novo Parkinson's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International journal of Alzheimer's disease"],["dc.bibliographiccitation.volume","2010"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2019-07-09T11:53:09Z"],["dc.date.available","2019-07-09T11:53:09Z"],["dc.date.issued","2010"],["dc.description.abstract","We studied the diagnostic value of CSF Aβ42/tau versus low Aβ1-42% and high Aβ1-40(ox)% levels for differential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), respectively. CSF of 45 patients with AD, 15 with DLB, 21 with Parkinson's disease dementia (PDD), and 40 nondemented disease controls (NDC) was analyzed by Aβ-SDS-PAGE/immunoblot and ELISAs (Aβ42 and tau). Aβ42/tau lacked specificity in discriminating AD from DLB and PDD. Best discriminating biomarkers were Aβ1-42% and Aβ1-40(ox)% for AD and DLB, respectively. AD and DLB could be differentiated by both Aβ1-42% and Aβ1-40(ox)% with an accuracy of 80% at minimum. Thus, we consider Aβ1-42% and Aβ1-40(ox)% to be useful biomarkers for AD and DLB, respectively. We propose further studies on the integration of Aβ1-42% and Aβ1-40(ox)% into conventional assay formats. Moreover, future studies should investigate the combination of Aβ1-40(ox)% and CSF alpha-synuclein for the diagnosis of DLB."],["dc.identifier.doi","10.4061/2010/761571"],["dc.identifier.fs","575758"],["dc.identifier.pmid","20862375"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60350"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-0252"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Combined Analysis of CSF Tau, Aβ42, Aβ1-42% and Aβ1-40% in Alzheimer's Disease, Dementia with Lewy Bodies and Parkinson's Disease Dementia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]