Evidence map›Paper›PMID 39051027›Full record

ArticleBrain communications2024

Plasma pTau181 and pTau217 predict asymptomatic amyloid accumulation equally well as amyloid PET.

Steffi De Meyer, Jolien M Schaeverbeke, Emma S Luckett, Mariska Reinartz, Elena R Blujdea, Isabelle Cleynen, Patrick Dupont, Koen Van Laere, Jeroen Vanbrabant, Erik Stoops and 7 more

Abstract read
In one paragraph

Article in Brain communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Plasma P-tau217 for detecting amyloid clearance after donanemab in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  2. Trial
  3. Article
  4. Article
  5. [Dementia with Lewy bodies].Fortschritte der Neurologie-Psychiatrie · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Predicting Preclinical Cognitive Decline Using Plasma P-tau217 andmedRxiv : the preprint server for health sciences · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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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

17 authors.

Steffi De MeyerLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0001-6729-7601
Jolien M SchaeverbekeLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.
Emma S LuckettLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0003-1777-4742
Mariska ReinartzLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0001-7964-7963
Elena R BlujdeaNeurochemistry Laboratory, Department of Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, 1081 HV Amsterdam, The Netherlands.
Isabelle CleynenLaboratory for Complex Genetics, Department of Human Genetics, KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0003-0857-7683
Patrick DupontLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.
Koen Van LaereNuclear Medicine and Molecular Imaging, Department of Imaging and Pathology, KU Leuven, 3000 Leuven, Belgium.
Jeroen VanbrabantADx NeuroSciences NV, 9052 Ghent, Belgium.
Erik StoopsADx NeuroSciences NV, 9052 Ghent, Belgium.
Eugeen VanmechelenADx NeuroSciences NV, 9052 Ghent, Belgium.
Guglielmo di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, S-431 80 Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, S-431 80 Mölndal, Sweden.ORCID https://orcid.org/0000-0003-3930-4354
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, S-431 80 Mölndal, Sweden.
Charlotte E TeunissenNeurochemistry Laboratory, Department of Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, 1081 HV Amsterdam, The Netherlands.ORCID https://orcid.org/0000-0002-4061-0837
Koen PoesenLaboratory for Molecular Neurobiomarker Research, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0001-5290-9476
Rik VandenbergheLaboratory for Cognitive Neurology, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven, 3000 Leuven, Belgium.ORCID https://orcid.org/0000-0001-6237-2502

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dynamic phase of preclinical Alzheimer's disease, as characterized by accumulating cortical amyloid-β, is a window of opportunity for amyloid-β-lowering therapies to have greater efficacy. Biomarkers that accurately predict amyloid-β accumulation may be of critical importance for participant inclusion in secondary prevention trials and thus enhance development of early Alzheimer's disease therapies. We compared the abilities of baseline plasma pTau181, pTau217 and amyloid-β PET load to predict future amyloid-β accumulation in asymptomatic elderly. In this longitudinal cohort study, baseline plasma pTau181 and pTau217 were quantified using single molecule array assays in cognitively unimpaired elderly selected from the community-recruited F-PACK cohort based on the availability of baseline plasma samples and longitudinal amyloid-β PET data (median time interval = 5 years, range 2-10 years). The predictive abilities of pTau181, pTau217 and PET-based amyloid-β measures for PET-based amyloid-β accumulation were investigated using receiver operating characteristic analyses, correlations and stepwise regression analyses. We included 75 F-PACK subjects (mean age = 70 years, 48% female), of which 16 were classified as amyloid-β accumulators [median (interquartile range) Centiloid rate of change = 3.42 (1.60) Centiloids/year). Plasma pTau181 [area under the curve (95% confidence interval) = 0.72 (0.59-0.86)] distinguished amyloid-β accumulators from non-accumulators with similar accuracy as pTau217 [area under the curve (95% confidence interval) = 0.75 (0.62-0.88) and amyloid-β PET [area under the curve (95% confidence interval) = 0.72 (0.56-0.87)]. Plasma pTau181 and pTau217 strongly correlated with each other (

Indexed as

amyloid PETbiomarkersbloodphosphorylated taupreclinical Alzheimer’s disease

Identifiers

PMID39051027
PMCPMC11267224

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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.