Evidence map›Paper›PMID 42169160›Full record

ArticleAlzheimer's research & therapy2026

Longitudinal plasma p-tau217 as a marker for tracking progression and predicting cognitive decline in Alzheimer's disease.

Jehyun Ahn, Jihwan Yun, Michael W Weiner, Daeun Shin, Heekyoung Kang, Sohyun Yim, Seonghyeon Kim, Heekyoung Park, Hyemin Jang, Min Young Chun and 6 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Jehyun Ahn *Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Jihwan Yun *Department of Neurology, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul, Republic of Korea.
Michael W WeinerDepartment of Radiology, University of California San Francisco, 505 Parnassus Avenue #001, San Francisco, CA, 94117, USA.
Daeun ShinDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Heekyoung KangDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Sohyun YimDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Seonghyeon KimDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Heekyoung ParkDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Hyemin JangDepartment of Neurology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-Ro 43-Gil, Songpa-Gu, Seoul, 05505, Republic of Korea.
Min Young ChunDepartment of Neurology, Yonsei University College of Medicine, Seoul, South Korea.
Eun Hye LeeDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Hee Jin KimDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Duk L NaDepartment of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Jun Pyo Kim *Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea. torch0703@gmail.com.
Sang Won Seo *Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea. sw72.seo@samsung.com.
ADNI study group

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
Institute of Information & Communications Technology Planning & Evaluation RS-2021-II212068Korea Dementia Research Center RS-2020-KH106434Korea Health Industry Development Institute RS-2025-02223212Korea National Institute of Health 2024-ER1003-01National Research Foundation of Korea RS-2019-NR040057NIA NIH HHS U01 AG024904Samsung Medical Center, Sungkyunkwan University SMX1250081
6 · The paper itself

Abstract

backgroundPlasma phosphorylated tau217 (p-tau217) is a promising biomarker for Alzheimer's disease (AD) with strong cross-sectional concordance with beta-amyloid (Aβ) and tau pathology. However, its longitudinal behavior across disease stages and assay platforms, and its prognostic value for cognitive decline according to Aβ status, remain insufficiently characterized. This study aimed to evaluate stage- and assay-specific longitudinal changes in plasma p-tau217 and to determine their utility for predicting cognitive decline.

methodsWe analyzed longitudinal data from 393 participants in the NA-ADNI, including cognitively unimpaired (CU) and cognitively impaired (CI) individuals. Plasma p-tau217 was measured using five assay platforms. Linear mixed-effects models were used to assess longitudinal biomarker trajectories, with time as the primary predictor and random intercepts and slopes. Aβ status and time-by-Aβ interactions were included to examine differential trajectories. Annualized biomarker changes were derived and related to longitudinal cognitive outcomes using models of Clinical Dementia Rating-Sum of boxes (CDR-SB) scores. Marginal R

resultsPlasma p-tau217 levels increased significantly over time across all assay platforms in both CU and CI groups (all q < 0.05). The largest standardized time effects were observed for the ALZpath-Simoa assay (β

conclusionsLongitudinal plasma p-tau217 is a robust marker of AD progression, but its optimal prognostic application depends on cognitive stage, Aβ status, and assay platform. These findings support stage-specific strategies for using serial plasma biomarkers in clinical monitoring and therapeutic trials.

Indexed as

Alzheimer DiseaseCognitive Dysfunctiontau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersDisease ProgressionFemaleHumansLongitudinal StudiesMalePhosphorylationAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseCognitive declineLongitudinal analysisPlasma biomarkersP-tau217

Identifiers

PMID42169160
PMCPMC13404311

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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.