Evidence map›Paper›PMID 41117398›Full record

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

Predicting cognitive decline with amyloid-PET, plasma p-tau217, Aβ42/40, and p-tau217/Aβ42 in a community-based cohort - relevance for clinical trial enrollment.

Dario Bachmann, Maha Wybitul, Andreas Buchmann, Christoph Gericke, Antje Saake, Sandro Studer, Katrin Rauen, Esmeralda Gruber, Kaj Blennow, Henrik Zetterberg and 4 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
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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

14 authors.

Dario BachmannInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-2863-537X
Maha WybitulInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Andreas BuchmannInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Christoph GerickeInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Antje SaakeInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Sandro StuderInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Katrin RauenInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Esmeralda GruberInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Roger M NitschInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Christoph HockInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Valerie TreyerInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.
Anton GietlInstitute for Regenerative Medicine, University of Zurich, Zurich, Switzerland.

Funding

AD Strategic Fund and the Alzheimer's Association ADSF-21-831376-CAD Strategic Fund and the Alzheimer's Association ADSF-21-831377-CAD Strategic Fund and the Alzheimer's Association ADSF-21-831381-CAD Strategic Fund and the Alzheimer's Association ADSF-24-1284328-CALF-agreement ALFGBG-715986ALF-agreement ALFGBG-965240Alzheimer's Association 2021 Zenith Award ZEN-21-848495Alzheimer's Association 2022-2025 SG-23-1038904 QCBluefield Project, Cure Alzheimer's FundEuropean Union Joint Program for Neurodegenerative Disorders JPND2019-466-236European Union Joint Programme - Neurodegenerative Disease Research JPND2021-00694European Union's Horizon Europe 101053962European Union's Horizon Europe Research 22HLT07Familjen Rönströms StiftelseHjärnfonden ALZ2022-0006Hjärnfonden FO2017-0243Kirsten and Freddy Johansen Foundation 2019-02397Kirsten and Freddy Johansen Foundation 2022-01018Kirsten and Freddy Johansen Foundation 2023-00356La Fondation Recherche AlzheimerMäxi FoundationNational Institute for Health and Care Research University College London Hospitals Biomedical Research CentreOlav Thon FoundationStiftelsen för Gamla Tjänarinnor FO2022-0270Swedish Alzheimer Foundation AF-930351Swedish Alzheimer Foundation AF-939721Swedish Alzheimer Foundation AF-968270Swedish Alzheimer Foundation AF-994551Swedish State Support for Clinical Research ALFGBG-71320Swiss National Science Foundation 10000763the Erling-Persson Family Foundationthe Swedish Research Council 2017-00915the Swedish Research Council 2022-00732UK Dementia Research Institute UKDRI-1003University of ZurichVontobel Foundation
6 · The paper itself

Abstract

introductionIdentifying at-risk individuals and selecting sensitive cognitive outcome measures are critical for designing efficient clinical trials targeting early Alzheimer's disease (AD) stages.

methodsWe compared amyloid beta (Aβ)-positron emission tomography (PET), plasma tau phosphorylated at threonine 217 (p-tau217), Aβ42/40, and p-tau217/Aβ42-related decline across neuropsychological and functional measures in 225 individuals (176 cognitively unimpaired (CU), 49 with mild cognitive impairment (MCI). Johnson-Neyman analysis identified the biomarkers, which were used as trial inclusion criteria to estimate sample sizes needed to detect a 30% slowing across cognitive outcomes.

resultsIn the CU, using combined plasma Aβ42/40 and p-tau217 cut-offs for eligibility yielded the lowest sample size estimates for a comprehensive multidomain cognitive composite score, whereas sample sizes were higher for all other inclusion criteria based on single biomarkers. In MCI, estimates were substantially lower and less variable across most inclusion criteria and outcome measures. DISCUSSION: These findings highlight the need for careful consideration of outcome measures, baseline diagnosis, and inclusion criteria, given their substantial effect on sample size estimation in trials. HIGHLIGHTS: Aβ SUVR, plasma p-tau217, and the p-tau217/Aβ42 ratio predicted decline across multiple cognitive domains. Using cohort-specific biomarker cutoffs, sample size estimates were similar for p-tau217 combined with Aβ42/40 or Aβ SUVR. A multidomain composite best detected AD-related decline. Outcome measures and eligibility criteria strongly impact sample size estimates, especially in CU.

Indexed as

Amyloid beta-PeptidesCognitive DysfunctionPeptide Fragmentstau ProteinsAgedAged, 80 and overAlzheimer DiseaseBiomarkersCohort StudiesFemaleHumansMaleMiddle AgedNeuropsychological TestsPhosphorylationPositron-Emission TomographyAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide Fragmentstau Proteinsblood biomarkersclinical trialscognitioncomposite scorepreclinical Alzheimer's diseasesample size

Identifiers

PMID41117398
PMCPMC12538628

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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.