Klafki, Hans-Wolfgang

[["dc.bibliographiccitation.artnumber","94"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Aichholzer, Freyja"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Ogorek, Isabella"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Scherbaum, Norbert"],["dc.contributor.author","Weggen, Sascha"],["dc.contributor.author","Wirths, Oliver"],["dc.date.accessioned","2021-11-25T11:07:12Z"],["dc.date.accessioned","2022-08-18T12:39:08Z"],["dc.date.available","2021-11-25T11:07:12Z"],["dc.date.available","2022-08-18T12:39:08Z"],["dc.date.issued","2021-05-04"],["dc.date.updated","2022-07-29T12:17:48Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Alzheimer’s disease (AD) is a neurodegenerative disorder associated with extracellular amyloid-β peptide deposition and progressive neuron loss. Strong evidence supports that neuroinflammatory changes such as the activation of astrocytes and microglia cells are important in the disease process. Glycoprotein nonmetastatic melanoma protein B (GPNMB) is a transmembrane glycoprotein that has recently been associated with an emerging role in neuroinflammation, which has been reported to be increased in post-mortem brain samples from AD and Parkinson’s disease patients.\r\n \r\n \r\n Methods\r\n The present study describes the partial “fit for purpose” validation of a commercially available immunoassay for the determination of GPNMB levels in the cerebrospinal fluid (CSF). We further assessed the applicability of GPNMB as a potential biomarker for AD in two different cohorts that were defined by biomarker-supported clinical diagnosis or by neuroimaging with amyloid positron emission tomography, respectively.\r\n \r\n \r\n Results\r\n The results indicated that CSF GPNMB levels could not distinguish between AD or controls with other neurological diseases but correlated with other parameters such as aging and CSF pTau levels.\r\n \r\n \r\n Conclusions\r\n The findings of this study do not support GPNMB in CSF as a valuable neurochemical diagnostic biomarker of AD but warrant further studies employing healthy control individuals."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.citation","Alzheimer's Research & Therapy. 2021 May 04;13(1):94"],["dc.identifier.doi","10.1186/s13195-021-00828-1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112967"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1758-9193"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Alzheimer’s disease"],["dc.subject","GPNMB"],["dc.subject","Cerebrospinal fluid"],["dc.subject","Biomarker"],["dc.subject","Inflammation"],["dc.subject","Immunoassay"],["dc.title","Evaluation of cerebrospinal fluid glycoprotein NMB (GPNMB) as a potential biomarker for Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","127"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Klafki, Hans-W."],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Manuilova, Ekaterina"],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Jethwa, Alexander"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Jahn-Brodmann, Anke"],["dc.contributor.author","Osterloh, Dirk"],["dc.contributor.author","Lachmann, Ingolf"],["dc.contributor.author","Breitling, Benedict"],["dc.contributor.author","Rauter, Carolin"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Palme, Stefan"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2022-09-12T07:56:44Z"],["dc.date.available","2022-09-12T07:56:44Z"],["dc.date.issued","2022-09-07"],["dc.date.updated","2022-09-11T03:10:27Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Measurements of the amyloid-β (Aβ) 42/40 ratio in blood plasma may support the early diagnosis of Alzheimer’s disease and aid in the selection of suitable participants in clinical trials. Here, we compared the diagnostic performance of fully automated prototype plasma Aβ42/40 assays with and without pre-analytical sample workup by immunoprecipitation.\r\n \r\n \r\n Methods\r\n A pre-selected clinical sample comprising 42 subjects with normal and 38 subjects with low cerebrospinal fluid (CSF) Aβ42/40 ratios was studied. The plasma Aβ42/40 ratios were determined with fully automated prototype Elecsys® immunoassays (Roche Diagnostics GmbH, Penzberg, Germany) by direct measurements in EDTA plasma or after pre-analytical Aβ immunoprecipitation. The diagnostic performance for the detection of abnormal CSF Aβ42/40 was analyzed by receiver operating characteristic (ROC) analysis. In an additional post hoc analysis, a biomarker-supported clinical diagnosis was used as a second endpoint.\r\n \r\n \r\n Results\r\n Pre-analytical immunoprecipitation resulted in a significant increase in the area under the ROC curve (AUC) from 0.73 to 0.88 (p = 0.01547) for identifying subjects with abnormal CSF Aβ42/40. A similar improvement in the diagnostic performance by pre-analytical immunoprecipitation was also observed when a biomarker-supported clinical diagnosis was used as a second endpoint (AUC increase from 0.77 to 0.92, p = 0.01576).\r\n \r\n \r\n Conclusions\r\n Our preliminary observations indicate that pre-analytical Aβ immunoprecipitation can improve the diagnostic performance of plasma Aβ assays for detecting brain amyloid pathology. The findings may aid in the further development of blood-based immunoassays for Alzheimer’s disease ultimately suitable for screening and routine use."],["dc.identifier.citation","Alzheimer's Research & Therapy. 2022 Sep 07;14(1):127"],["dc.identifier.doi","10.1186/s13195-022-01071-y"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114202"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Alzheimer’s disease"],["dc.subject","Biomarker assay"],["dc.subject","Plasma Amyloid-β 42/40"],["dc.subject","Immunoprecipitation"],["dc.subject","Pre-analytical sample workup"],["dc.title","Diagnostic performance of automated plasma amyloid-β assays combined with pre-analytical immunoprecipitation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]