Wiltfang, Jens

[["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","96"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fluids and Barriers of the CNS"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Morgado, Barbara"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2022-12-05T09:15:24Z"],["dc.date.available","2022-12-05T09:15:24Z"],["dc.date.issued","2022-12-03"],["dc.date.updated","2022-12-04T04:11:01Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n A reduced amyloid-β (Aβ)42/40 peptide ratio in blood plasma represents a peripheral biomarker of the cerebral amyloid pathology observed in Alzheimer’s disease brains. The magnitude of the measurable effect in plasma is smaller than in cerebrospinal fluid, presumably due to dilution by Aβ peptides originating from peripheral sources. We hypothesized that the observable effect in plasma can be accentuated to some extent by specifically measuring Aβ1–42 and Aβ1–40 instead of AβX–42 and AβX–40.\r\n \r\n \r\n Methods\r\n We assessed the plasma AβX–42/X–40 and Aβ1–42/1–40 ratios in an idealized clinical sample by semi-automated Aβ immunoprecipitation followed by closely related sandwich immunoassays. The amyloid-positive and amyloid-negative groups (dichotomized according to Aβ42/40 in cerebrospinal fluid) were compared regarding the median difference, mean difference, standardized effect size (Cohen’s d) and receiver operating characteristic curves. For statistical evaluation, we applied bootstrapping.\r\n \r\n \r\n Results\r\n The median Aβ1–42/1–40 ratio was 20.86% lower in amyloid-positive subjects than in the amyloid-negative group, while the median AβX–42/X–40 ratio was only 15.56% lower. The relative mean difference between amyloid-positive and amyloid-negative subjects was −18.34% for plasma Aβ1–42/1–40 compared to −15.50% for AβX–42/X–40. Cohen’s d was 1.73 for Aβ1–42/1–40 and 1.48 for plasma AβX–42/X–40. Unadjusted p-values < 0.05 were obtained after .632 bootstrapping for all three parameters. Receiver operating characteristic analysis indicated very similar areas under the curves for plasma Aβ1–42/1–40 and AβX–42/X–40.\r\n \r\n \r\n Conclusions\r\n Our findings support the hypothesis that the relatively small difference in the plasma Aβ42/40 ratio between subjects with and without evidence of brain amyloidosis can be accentuated by specifically measuring Aβ1–42/1–40 instead of AβX–42/X–40. A simplified theoretical model explaining this observation is presented."],["dc.identifier.citation","Fluids and Barriers of the CNS. 2022 Dec 03;19(1):96"],["dc.identifier.doi","10.1186/s12987-022-00390-4"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118429"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Alzheimer’s disease"],["dc.subject","Biomarker"],["dc.subject","Amyloid-β peptides"],["dc.subject","Blood plasma"],["dc.subject","Aβ42/40 ratio"],["dc.subject","Immunoassay"],["dc.title","Is plasma amyloid-β 1–42/1–40 a better biomarker for Alzheimer’s disease than AβX–42/X–40?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]