Evidence map›Paper›PMID 40588692›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Plasma p-tau231 in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: A cross-sectional and longitudinal cohort study.

Vincent Malotaux, Nicholas J Ashton, Annika Öhrfelt, Yinghua Chen, Yi Su, Gloria Garcia-Ospina, Claudia Guzman-Martínez, Andres Villegas-Lanau, Johana Gómez-Ramirez, Margarita Giraldo-Chica and 16 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Observational
  2. Article
  3. 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

26 authors.

Vincent MalotauxMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0003-0737-9220
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Inst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Annika ÖhrfeltDepartment of Psychiatry and Neurochemistry, Inst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Yinghua ChenBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Yi SuBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Gloria Garcia-OspinaGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Claudia Guzman-MartínezGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Andres Villegas-LanauGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Johana Gómez-RamirezGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Margarita Giraldo-ChicaGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
David AguillonGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Victoria TiradoGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Ana BaenaGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Claudia MunozGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Natalia Acosta-BaenaGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Jeremy J PruzinBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Valentina GhisaysBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Silvia Rios-RomenetsGrupo de Neurociencias de Antioquia, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Clara Vila-CastelarMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jairo E MartínezMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Averi GiudicessiMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Pierre N TariotBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Inst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Kaj BlennowClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Eric M ReimanBanner Alzheimer's Institute, Phoenix, Arizona, USA.
Yakeel T QuirozMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Funding

Alzheimer's Prevention Initiative (API) Autosomal Dominant AD TrialNIA NIH HHSNIH/NIANINDS NIH HHS
6 · The paper itself

Abstract

introductionPlasma phosphorylated tau (p-tau)-231 is a promising biomarker for Alzheimer's disease (AD), particularly in preclinical stages. We evaluated its diagnostic value in presenilin 1 (PSEN1) E280A mutation carriers versus non-carriers and compared it to p-tau217 and neurofilament light chain (NfL).

methodsWe analyzed plasma p-tau231 in 722 carriers and 640 non-carriers (ages 18-75). Longitudinal data from 164 carriers and 132 non-carriers were available, with 137 carriers and 109 non-carriers having p-tau231, p-tau217, and NfL levels. Analyses used linear mixed effects models and restricted cubic splines.

resultsE280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001). Baseline p-tau231 levels correlated with age, distinguishing carriers at age 23. Rates of change differed at age 19, ≈ 25 years before cognitive impairment. In a subset, p-tau231 changes differentiated carriers by age 20, earlier than p-tau217 and NfL. DISCUSSION: Plasma p-tau231 is a sensitive biomarker for early AD detection and progression monitoring. HIGHLIGHTS: Plasma phosphorylated tau (p-tau)231 levels are associated with age in presenilin 1 carriers and non-carriers. Baseline p-tau231 levels diverged between carriers and non-carriers at age 23. Plasma p-tau231 changes distinguished carriers by age 19, at very early stages. P-tau231 longitudinal changes differentiate carriers earlier than p-tau217 or neurofilament light chain.

Indexed as

Alzheimer DiseasePresenilin-1tau ProteinsAdultAgedBiomarkersCohort StudiesCross-Sectional StudiesFemaleHumansLongitudinal StudiesMaleMiddle AgedMutationNeurofilament ProteinsPhosphorylationBiomarkersneurofilament protein LNeurofilament ProteinsPresenilin-1PSEN1 protein, humantau ProteinsAlzheimer's disease, autosomal dominant Alzheimer's diseasebiomarkers, plasma, presenilin 1, phosphorylated tau231

Identifiers

PMID40588692
PMCPMC12208796

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Registered trials

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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.