Evidence map›Paper›PMID 41339948›Full record

ArticleAlzheimer's research & therapy2025

Individualized prediction of clinical progression to dementia using plasma biomarkers in non-demented elderly.

Madison I J Honey, Ingrid S van Maurik, Argonde C van Harten, Mariam Gouda, Mardou van Leeuwenstijn, Arenda Mank, Calvin Trieu, Vincent Bouteloup, Geneviève Chêne, Isabelle Pellegrin and 9 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

19 authors.

Madison I J HoneyDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands. m.i.j.honey@amsterdamumc.nl.
Ingrid S van MaurikDepartment of Epidemiology and Data Science, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam, The Netherlands.
Argonde C van HartenDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Mariam GoudaDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Mardou van LeeuwenstijnDepartment of Neurology, Alzheimer Center Amsterdam, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Arenda MankDepartment of Neurology, Alzheimer Center Amsterdam, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Calvin TrieuDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Vincent BouteloupInserm UMR1219 and CIC 1401 EC, Pôle Santé Publique, University of Bordeaux, Bordeaux Population Health, Centre Hospitalier Universitaire (CHU) de Bordeaux, Bordeaux, France.
Geneviève ChêneInserm UMR1219 and CIC 1401 EC, Pôle Santé Publique, University of Bordeaux, Bordeaux Population Health, Centre Hospitalier Universitaire (CHU) de Bordeaux, Bordeaux, France.
Isabelle PellegrinInserm UMR1219 and CIC 1401 EC, Pôle Santé Publique, University of Bordeaux, Bordeaux Population Health, Centre Hospitalier Universitaire (CHU) de Bordeaux, Bordeaux, France.
Carole DufouilInserm UMR1219 and CIC 1401 EC, Pôle Santé Publique, University of Bordeaux, Bordeaux Population Health, Centre Hospitalier Universitaire (CHU) de Bordeaux, Bordeaux, France.
James D DoeckeCSIRO Health and Biosecurity/Australian E-Health Research Centre, Herston, QLD, Australia.
Christopher J FowlerThe Florey Institute, The University of Melbourne, Parkville, VIC, Australia.
Colin L MastersThe Florey Institute, The University of Melbourne, Parkville, VIC, Australia.
Yolande PijnenburgDepartment of Neurology, Alzheimer Center Amsterdam, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
David WilsonQuanterix Corporation, Billerica, MA, USA.
Wiesje M van der FlierDepartment of Neurology, Alzheimer Center Amsterdam, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Charlotte E TeunissenDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Inge M W VerberkDepartment of Laboratory Medicine, Neurochemistry Laboratory, Amsterdam University Medical Centers, Vrije Universiteit, Amsterdam Neuroscience, Amsterdam, The Netherlands.

Funding

Alzheimer Nederland WE.09-20921-04
6 · The paper itself

Abstract

backgroundWe aimed to develop individualized predictions for risk of developing any-cause dementia and Alzheimer's disease (AD) dementia, in individuals with subjective cognitive decline (SCD) or mild cognitive impairment (MCI), using plasma phosphorylated-tau-181 (pTau181), phosphorylated-tau-217 (pTau217; in a subset), amyloid beta1-42/1-40 (Aβ42/40), glial fibrillary acidic protein (GFAP) and/or neurofilament light (NfL).

methodsFrom the Amsterdam Dementia Cohort we included 314 individuals with SCD (age 61 ± 9 years, n = 184 (59%) male, MMSE 29 ± 1) and 253 individuals with MCI (age 65 ± 7 years, n = 165 (65%) male, MMSE 27 ± 2), who had annual follow-up (median duration 2.4 years). Cox proportional hazards regression models were used to calculate probabilities for progression to dementia and were externally validated in MEMENTO and AIBL cohorts.

resultsDuring follow-up 20 SCD and 99 MCI patients developed dementia. For MCI patients who progressed to any form of dementia, plasma GFAP contributed on top of age, sex, and MMSE score in the parsimonious individualized prognostic model (C-index = 0.69 [95%CI = 0.63; 0.76]). With AD-dementia as the outcome, GFAP and pTau181 were selected in the parsimonious model on top of the demographic variables (C-index = 0.71 [95%CI = 0.65; 0.76]). In the subset of 197 MCI individuals with pTau217 measurements, pTau217 was selected in the parsimonious model on top of the demographic variables (C-index = 0.75 [95%CI = 0.69; 0.79]). External validation demonstrated that the models are robust in a memory clinic setting.

conclusionsOur prediction models have utility for clinical practice to calculate progression probabilities for development of dementia in individual patients living with MCI over a 1-, 3- and 5-year time period.

Indexed as

Cognitive DysfunctionDementiaAgedAmyloid beta-PeptidesBiomarkersCohort StudiesDisease ProgressionFemaleFollow-Up StudiesGlial Fibrillary Acidic ProteinHumansMaleMiddle AgedNeurofilament ProteinsPeptide Fragmentstau ProteinsAmyloid beta-PeptidesBiomarkersGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlzheimer’s diseaseBiomarkersBloodDementiaIndividualisedMild cognitive impairmentPlasmaPrognosisRiskSubjective cognitive decline

Identifiers

PMID41339948
PMCPMC12781432

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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.