Evidence map›Paper›PMID 42437975›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Proteomics of post mortem brains in early- and late-onset Alzheimer's disease: Unraveling differential Aβ effects and potential AD biomarkers.

Evangelia Thanou, Andrea Ganz, Débora Pita-Illobre, Frank Koopmans, Jeroen J M Hoozemans, Annemieke Rozemuller, Henne Holstege, August B Smit, Ka Wan Li

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Evangelia ThanouDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.ORCID https://orcid.org/0000-0001-6843-4591
Andrea GanzDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Débora Pita-IllobreDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Frank KoopmansDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Jeroen J M HoozemansDepartment of Pathology, Amsterdam Neuroscience, Amsterdam UMC, Amsterdam, The Netherlands.
Annemieke RozemullerDepartment of Pathology, Amsterdam Neuroscience, Amsterdam UMC, Amsterdam, The Netherlands.
Henne HolstegeDepartment of Clinical Genetics, Amsterdam Neuroscience, Amsterdam UMC, Amsterdam, The Netherlands.
August B SmitDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Ka Wan LiDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.

Funding

Dutch Research Council (NWO) OCENW.KLEIN.558EU Marie Curie ITN EuroNeurotrophin 765704OPD-ZonMW via the MODEM consortium
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) occurs primarily as late‑onset (LOAD) and less frequently as early‑onset (EOAD). Its defining pathologies are hyperphosphorylated tau tangles and amyloid beta (Aβ) plaques.

methodsWe analyzed the proteomes of 115 post mortem temporal lobe samples by mass spectrometry and searched with a dedicated AD spectral library including tau post‑translational modifications and Aβ isoforms to examine global protein changes in LOAD and EOAD.

resultsAD tissues showed mitochondrial and synaptic pathway downregulation and immune and small‑molecule metabolic process upregulation, with EOAD exhibiting larger fold changes. AD biomarkers were elevated, and two multi‑phosphorylated tau peptides (p‑tau231/p-tau235 and p-tau231/p-tau235/p-tau237) were detected predominantly in AD. Aβ was present in 45% of cognitively unimpaired elderly controls, with subtle proteome changes resembling an early stage of neurodegeneration. DISCUSSION: EOAD appears more aggressive. Tau p-tau231/p-tau235 and p-tau231/p-tau235/p-tau237 hold promise as novel AD biomarkers. Aβ's detection in cognitively unimpaired elderly controls precedes clinical AD symptoms.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainProteomicsAgedAged, 80 and overAge of OnsetAutopsyBiomarkersFemaleHumansMalePhosphorylationProteometau ProteinsAmyloid beta-PeptidesBiomarkersProteometau ProteinsAβbiomarkersearly‐onset Alzheimer's diseaseglobal protein changeslate‐onset Alzheimer's diseasephosphorylated tauproteomics

Identifiers

PMID42437975
PMCPMC13357694

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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.