ArticleNeurology2026
Performance of Alzheimer Disease Plasma Biomarkers in Patients With Prion Diseases.
Article in Neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Prion disease mimicking rapidly progressive Alzheimer disease: case series and systematic review.Journal of neurology · 2026Pooled it
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18 authors.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesPrion diseases can mimic Alzheimer disease (AD) at presentation. Alzheimer's Association AD diagnostic criteria suggest that a single abnormal highly specific plasma biomarker (including p-tau217) is sufficient for a biological diagnosis. We investigated the performance of AD plasma biomarkers in distinguishing AD and prion diseases.
methodsWe examined plasma biomarker data from patients with prion disease from a prospective cohort study recruited through the UK National Prion Clinic. Prion diseases were diagnosed clinically or with autopsy confirmation, and AD was diagnosed clinically with CSF biomarker confirmation. Plasma p-tau217, p-tau181, Aβ42/40 ratio, brain-derived tau (BD-tau), neurofilament light chain (NfL), and glial fibrillary acid protein (GFAP) were measured using Simoa. Median biomarker values in different groups were compared with Kruskal-Wallis test, and area under the receiver operating characteristic curve was used to compare accuracy in distinguishing prion diseases from sporadic AD (sAD). Lumipulse p-tau217 and NfL were measured in a validation study in a different laboratory.
resultsIn the main study, we analyzed 345 samples from 278 individuals (mean age 58 [SD 13.5], 48.2% female), including 204 with prion diseases (121 sporadic Creutzfeldt-Jakob disease [CJD], 11 iatrogenic CJD, 9 variant CJD, 47 slow-progressing inherited prion disease (IPD) and 16 fast-progressing IPD), 33 with AD, and 41 healthy controls. For discriminating prion disease without AD copathology from sAD, none of p-tau217 (area under the curve [AUC] [95% CI] 0.605 [0.486-0.724]), p-tau181 (AUC 0.554 [0.446-0.661]), or GFAP (AUC 0.514 [0.389-0.640]) performed well. Aβ42/40 discriminated moderately (AUC 0.770 [0.684-0.856]). NfL/p-tau217 ratio (AUC 0.996 [0.987-1.000]), NfL (AUC 0.988 [0.974-1.000]), BD-tau/p-tau217 ratio (AUC 0.963 [0.929-0.996]), and BD-tau (AUC 0.934 [0.890-0.978]) discriminated very well. In an independent validation study, consecutive samples were analyzed from 32 patients with sAD and 35 patients with sporadic Creutzfeldt-Jakob disease (mean age 65.0 [SD 6.4], 56.7% female). NfL/p-tau217 again discriminated almost perfectly (AUC 0.986 [95% CI 0.966-1.000]). DISCUSSION: Plasma p-tau217 and p-tau181 are increased in both AD and prion diseases (regardless of burden of AD copathology). Diagnosing AD with a single abnormal p-tau plasma biomarker risks misdiagnosing prion diseases as AD. Plasma NfL/p-tau217 discriminates near-perfectly and could act as a flag to suspect prion diseases where this is a diagnostic possibility. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that plasma NfL/p-tau217 discriminates patients with CJD from those with AD.
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