Evidence map›Paper›PMID 41078215›Full record

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

Differential effects of age and sex on tau pathology propagation in the htau mouse model: A neuropathological and proteomic study.

Andreea-Claudia Kosa, Lidia Lopez-Gutierrez, Kunie Ando, Emilie Doeraene, Emmanuel Aydin, Hinde Lasri, Alain Wathelet-Depauw, Karlien Pieters, David Van Morckhoven, Virginie Imbault and 6 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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Cells · 2026
    Article
  4. Review
  5. 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

16 authors.

Andreea-Claudia KosaAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Lidia Lopez-GutierrezAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Kunie AndoAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Emilie DoeraeneAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Emmanuel AydinAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Hinde LasriAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Alain Wathelet-DepauwAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Karlien PietersLaboratory of Clinical Cell Therapy, Université Libre de Bruxelles (ULB), Jules Bordet Institute, Brussels, Belgium.
David Van MorckhovenLaboratory of Clinical Cell Therapy, Université Libre de Bruxelles (ULB), Jules Bordet Institute, Brussels, Belgium.
Virginie ImbaultCytometry Core Facility, Medical Faculty, Université Libre de Bruxelles (ULB), Bruxelles, Belgium.
Christine DuboisCytometry Core Facility, Medical Faculty, Université Libre de Bruxelles (ULB), Bruxelles, Belgium.
Xavier BisteauCytometry Core Facility, Medical Faculty, Université Libre de Bruxelles (ULB), Bruxelles, Belgium.
Basile StamatopoulosLaboratory of Clinical Cell Therapy, Université Libre de Bruxelles (ULB), Jules Bordet Institute, Brussels, Belgium.
Mariana Igoillo-EsteveULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Jean-Pierre BrionAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.
Karelle LeroyAlzheimer and other tauopathies research group, ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, ULB Neuroscience Institute, Brussels, Belgium.

Funding

Belgian Fonds de la Recherche Scientifique MédicaleFondation Médicale Reine ElisabethFondation Recherche AlzheimerFonds De La Recherche Scientifique - FNRS FX47285Foundation Simone and Pierre ClerdentJaumotte-Demoulin FundKing Baudouin FoundationULB Génicot Fund
6 · The paper itself

Abstract

introductionAging is the main risk factor for Alzheimer's disease (AD), acting through still poorly understood mechanisms. AD is associated with the development of a tau pathology, a hallmark lesion propagating in the brain along neuroanatomically connected pathways. This study investigates changes in gene expression and patterns of tau pathology after induction of tau pathology propagation and the effects of age and sex on this propagation.

methodsYoung and old humanized htau mice were intracerebrally injected with pathological tau from human AD brain to induce tau pathology.

resultsYoung and old htau male mice showed similar patterns of tau pathology propagation, whereas the density of tau pathology was increased in young compared to old female mice. Proteomic analysis demonstrated differential expression of proteins involved in endocytosis, autophagosome formation, and tau splicing. DISCUSSION: The increased tau pathology formation in young female mice suggests that involvement of selected biological mechanisms could occur early in women during their midlife to explain their sensitivity to the development of tau pathology. HIGHLIGHTS: Tau pathology induced by human PHF-tau is mainly composed of 3R-tau in htau mice. Splicing factors favoring 4R-tau are downregulated in mice with tau pathology. Tau pathology propagation is increased in young females compared to old females. Proteins implicated in endocytosis and autophagy are modified when tau pathology propagates. Some protein expressions are similarly modified in young females and during normal aging.

Indexed as

AgingAlzheimer DiseaseBrainSex Characteristicstau ProteinsAge FactorsAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, TransgenicProteomicsSex Factorstau ProteinsagingAlzheimer's diseaseneurofibrillary tanglesproteomicsseedingtau pathology propagationtransgenic mouse

Identifiers

PMID41078215
PMCPMC12516240

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.