ArticleNeurology2026
Association of [
Article in Neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Atypical Alzheimer disease: a multi-axis framework toward defining heterogeneity.Nature reviews. Neurology · 2026Review
- Changes in five cerebrospinal fluid and three plasma Alzheimer's disease biomarkers across increasing brain amyloid-beta and tau pathology burden.Acta neuropathologica · 2026Article
- A probabilistic framework for clinicopathological Alzheimer's disease using tau-PET.Alzheimer's research & therapy · 2026Article
- Tau Biomarker-Based Diagnosis of Alzheimer Disease and the Anti-Abeta Therapeutic Window: Is There Overlap?Neurology · 2026Article
- Neuroimaging correlates and biomarker performance of a fully automated plasma p-tau217/Aβ42 ratio assay in a clinical cohort with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Celebrating neuropathology's contributions to Alzheimer's Disease Research Centers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
- Update ofAssociation of [2025
Authors and funding
18 authors.
Funding
Abstract
BACKGROUND AND
objectivesEvaluating tau biomarkers in patients with autopsy data is critical for validating their sensitivity and specificity to Alzheimer disease (AD) neuropathologic changes (ADNCs). We examined associations between [
methodsThis was a retrospective study conducted at the University of California San Francisco Neurodegenerative Disease Brain Bank that included all participants with a clinical diagnosis of neurodegenerative disease who underwent antemortem flortaucipir-PET and autopsy from 2013 to 2024. Flortaucipir-PET was acquired 80-100 minutes after injection and normalized to the inferior cerebellar cortex; standardized uptake value ratios (SUVRs) were extracted from the entorhinal cortex (early tau region) and the temporal meta-regions of interest (ROIs) (AD-signature region). Plasma p-tau217 was quantified using Simoa (Janssen) in 56 participants (median [interquartile range, IQR] PET-to-plasma duration: 1.6 months [0.24-3.7]). Semiquantitative rating of AD neurofibrillary tangle (NFT) burden in cortical areas was available for 56 participants. The diagnostic performance of tau PET and plasma p-tau217 was assessed using receiver operating characteristic analysis with cross-validation.
resultsWe analyzed 73 participants (median [IQR] age: 67 [59-73] years, 60% male, median [IQR] PET-to-autopsy duration: 3.9 [2.1-5.1] years) with primary neuropathologic diagnosis of AD (n = 39), frontotemporal lobar degeneration (tauopathies, n = 26; nontauopathies, n = 4), chronic traumatic encephalopathy (n = 2), and Lewy body disease (n = 2). Flortaucipir SUVRs were elevated in participants with a neuropathologic diagnosis of AD compared with non-AD participants. Consistently elevated PET signal was detected in both the entorhinal cortex and temporal meta-ROIs at NFT Braak stage VI and high ADNC levels. No PET signal elevation was observed at intermediate ADNC levels. AD NFT burden correlated with local flortaucipir SUVRs and plasma p-tau217 concentrations across cortical brain regions. Plasma p-tau217 concentrations increased at Braak stages V and VI and correlated with flortaucipir SUVRs ( DISCUSSION: Flortaucipir-PET and plasma p-tau217 both displayed strong specificity for primary AD neuropathologic diagnosis but limited sensitivity for early tau co-pathology in non-AD diagnoses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.