ArticleEBioMedicine2026
Detecting amyloid-β pathology in subjective cognitive decline using plasma and CSF biomarkers.
Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Dementia risk factors and biomarkers in subjective cognitive decline: real world evidence from the monza brain health service.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
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Authors and funding
29 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundSubjective cognitive decline (SCD) may represent an early stage of Alzheimer's disease (AD), but biomarker studies in this population are limited. Therefore, we compared the performance of a comprehensive panel of novel cerebrospinal fluid (CSF) and blood biomarkers across different platforms for detecting amyloid-β (Aβ) pathology in SCD.
methods143 individuals with SCD (20% Aβ-positive) from the β-AARC cohort were included. Aβ status was determined by CSF Aβ42/40. CSF and blood biomarkers of Aβ, tau, synaptic function, neurodegeneration, and glial reactivity were measured cross-sectionally.
findingsIn CSF, novel tau variants (p-tau205, p-tau217, p-tau231, p-tau235, NTA-tau) were elevated in Aβ-positive individuals with SCD. In plasma, p-tau217, p-tau217/Aβ42 (across multiple platforms), as well as p-tau181, p-tau181/Aβ42 and Aβ42/40 (platform-dependent) demonstrated strong discriminatory performance and high negative predictive value, but limited positive predictive value because of the low prevalence of Aβ pathology.
interpretationIn conclusion, several plasma biomarkers can exclude Aβ pathology in SCD, while some CSF and plasma markers indicate early AD-related changes. These plasma biomarkers could serve as accessible, cost-effective tools for early AD detection and risk stratification, and expedite the selection of candidates for disease-modifying treatments or preventive strategies.
fundingThe research leading to these results has received funding from the Alzheimer's Drug Discovery Foundation (ADDF) grants #RDADB-201906-2018897 and #201809-2016862. Additionally, the study has been funded by the Health Department of the Catalan Government, the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (Grant agreement No. 948677), and PI22/00456, funded by Instituto de Salud Carlos III (ISCIII).
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