Evidence map›Paper›PMID 40095069›Full record

ArticleActa neuropathologica2025

Biofluid-based staging of Alzheimer's disease.

Juan Lantero-Rodriguez, Laia Montoliu-Gaya, Nicholas J Ashton, Ilaria Pola, Joseph Therriault, Nesrine Rahmouni, Wagner S Brum, Stijn Servaes, Jenna Stevenson, Guglielmo Di Molfetta and 14 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Multivariate models using NULISAseq and plasma p-tau217 for staging Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  11. Review
  12. 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

24 authors.

Juan Lantero-Rodriguez *Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. juan.rodriguez.2@gu.se.
Laia Montoliu-Gaya *Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Ilaria PolaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Joseph TherriaultMontreal Neurological Institute, Montreal, QC, Canada.
Nesrine RahmouniMontreal Neurological Institute, Montreal, QC, Canada.
Wagner S BrumDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Stijn ServaesMontreal Neurological Institute, Montreal, QC, Canada.
Jenna StevensonMontreal Neurological Institute, Montreal, QC, Canada.
Guglielmo Di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Burak ArslanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Jesse KlostranecMontreal Neurological Institute, Montreal, QC, Canada.
Paolo VitaliMontreal Neurological Institute, Montreal, QC, Canada.
Maxime MontembeaultMontreal Neurological Institute, Montreal, QC, Canada.
Serge GauthierMontreal Neurological Institute, Montreal, QC, Canada.
Cecile TissotMontreal Neurological Institute, Montreal, QC, Canada.
Arthur C MacedoMontreal Neurological Institute, Montreal, QC, Canada.
Tharick A PascoalDepartment of Neurology and Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, USA.
Andreas JerominALZpath, Inc., Carlsbad, CA, USA.
Johan GobomDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Pedro Rosa-Neto *Montreal Neurological Institute, Montreal, QC, Canada.
Andrea L Benedet *Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Funding

Research Education ComponentP30AG072980 · NIA · BANNER HEALTH · PI Nicholas Ashton · 2021 to 2026
$24.9M
NIA NIH HHS P30 AG072980
6 · The paper itself

Abstract

Recently, conceptual systems for the in vivo staging of Alzheimer's disease (AD) using fluid biomarkers have been suggested. Thus, it is important to assess whether available fluid biomarkers can successfully stage AD into clinically and biologically relevant categories. In the TRIAD cohort, we explored whether p-tau217, p-tau205 and NTA-tau (biomarkers of early, intermediate and late AD pathology, respectively) have potential for biofluid-based staging in cerebrospinal fluid (CSF; n = 219) and plasma (n = 150), and compared them in a paired CSF and plasma subset (n = 76). Our findings suggest a good concordance between biofluid staging and underlying pathology when classifying amyloid-positivity into three categories based on neurofibrillary pathology: minimal/non-existent (p-tau217 positive), early-to-intermediate (p-tau217 and p-tau205 positivity), and advanced tau tangle deposition (p-tau217, p-tau205 and NTA-tau positive), as indexed by tau-PET. Discordant cases accounted for 4.6% and 13.3% of all CSF and plasma measurements respectively (9.2% and 11.8% in paired samples). Notably, CSF- and plasma-based staging matched one another in 61.7% of the cases, while approximately 32% of the remaining participants were one to three biofluid stages higher in CSF as compared to plasma. Overall, these exploratory results suggest that biofluid staging of AD holds potential for offering valuable insights into underlying AD hallmarks and disease severity. However, its applicability beyond molecular characterization at research settings has yet to be demonstrated.

Indexed as

Alzheimer Diseasetau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersCohort StudiesDisease ProgressionFemaleHumansMaleMiddle AgedNeurofibrillary TanglesPositron-Emission TomographyAmyloid beta-PeptidesBiomarkersMAPT protein, humantau ProteinsAlzheimerCSFPlasmap-TauStagingTau

Identifiers

PMID40095069
PMCPMC11913990

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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.