Evidence map›Paper›PMID 39907306›Full record

ArticleEuropean journal of neurology2025

Plasma Phosphorylated Tau 217 as a Discriminative Biomarker for Cerebral Amyloid Angiopathy.

Pei-Feng Hsieh, Hsin-Hsi Tsai, Chia-Ju Liu, Bo-Ching Lee, Ya-Chin Tsai, Ruoh-Fang Yen, Jiann-Shing Jeng, Li-Kai Tsai

Abstract read
In one paragraph

Article in European journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Biomarkers in preclinical and early Alzheimer's disease in China: a scoping review.The journal of prevention of Alzheimer's disease · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Clinical Management of Cerebral Amyloid Angiopathy.Journal of clinical medicine · 2025
    Review
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Pei-Feng HsiehDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.ORCID 0000-0003-2780-8897
Hsin-Hsi TsaiDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.ORCID 0000-0002-4721-1468
Chia-Ju LiuDepartment of Nuclear Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Bo-Ching LeeDepartment of Medical Imaging, National Taiwan University Hospital, Taipei, Taiwan.ORCID 0000-0002-1443-928X
Ya-Chin TsaiDepartment of Nuclear Medicine, National Taiwan University Hospital Hsin-Chu Branch, Hsin-Chu, Taiwan.
Ruoh-Fang YenDepartment of Nuclear Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Jiann-Shing JengDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Li-Kai TsaiDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.

Funding

National Science and Technology Council 112-2923-B-002-001-MY3National Science and Technology Council 113-2628-B-002-013-MY3National Taiwan University Hospital 113-N0075National Taiwan University Hospital 113-X0018
6 · The paper itself

Abstract

backgroundBlood-based biomarkers may offer a non-invasive approach to diagnose cerebral amyloid angiopathy (CAA), especially in early-stage. We evaluated the ability of plasma phosphorylated tau-217 (p-tau 217) to differentiate CAA from Alzheimer's disease (AD) and deep perforator arteriopathy (DPA).

methodsPatients with AD (age 73.7 ± 8.1 years), probable CAA (74.8 ± 6.9 years), or DPA (66.1 ± 10.4 years) were enrolled from memory and stroke clinics at a medical center in Taiwan. All participants received amyloid and tau PET scans. Plasma biomarkers were measured via a SIMOA immunoassay platform. The diagnostic utility of p-tau 217 was assessed using ROC analyses and the Youden cutoff. Associations between plasma p-tau 217 and neuroimaging variables in CAA were explored.

resultsPatients with CAA had lower plasma p-tau 217 (0.69 ± 0.76 vs. 1.28 ± 0.97 pg/mL, p < 0.001) and a lower p-tau 217/Aβ40 ratio (0.003 ± 0.002 vs. 0.006 ± 0.003, p < 0.001) than the AD group but higher levels than the DPA group (p-tau 217, 0.27 ± 0.13 pg/mL, p = 0.001; p-tau 217/Aβ40, 0.001 ± 0.0005, p < 0.001), although adjustment attenuated the difference in p-tau 217 between CAA and DPA. Plasma Aβ40, Aβ42, and Aβ40/Aβ42 were not significantly different between groups. Plasma p-tau 217 had moderate to good diagnostic utility to differentiate CAA vs. AD (sensitivity, 64.4%; specificity, 89.5%; AUC, 0.809) and CAA vs. DPA (sensitivity, 67.8%; specificity, 100%; AUC, 0.855). In CAA, p-tau 217 significantly correlated with the severity of CAA, amyloid PET signal intensity, and lobar microbleed count (p < 0.001).

conclusionsPlasma p-tau 217 may represent a non-invasive biomarker for distinguishing cerebral amyloid angiopathy (CAA) from other conditions, including AD and DPA.

Indexed as

Alzheimer DiseaseCerebral Amyloid Angiopathytau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersDiagnosis, DifferentialFemaleHumansMaleMiddle AgedPhosphorylationPositron-Emission TomographyAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer diseasecerebral amyloid angiopathycerebral small vessel diseasephosphorylated tau 217plasma biomarker

Identifiers

PMID39907306
PMCPMC11795418

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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.