Evidence map›Paper›PMID 42243402›Full record

ArticleNature neuroscience2026

Aberrant tau accumulation caused by MAPT mutations induces early pathological changes in axonal transport that are rescued by p38α inhibition.

Edoardo Moretto, Anna Masato, Chiara Panzi, André T Lopes, Skye Stuart, Samantha De La-Rocque, Maria Giuseppa Caso, Ian J White, Samuel S Harris, Marc Aurel Busche and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature neuroscience, 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

11 authors.

Edoardo MorettoUK Dementia Research Institute at University College London, London, UK. edoardo.moretto@cnr.it.ORCID http://orcid.org/0000-0002-3546-6797
Anna MasatoUK Dementia Research Institute at University College London, London, UK.
Chiara PanziUK Dementia Research Institute at University College London, London, UK.ORCID http://orcid.org/0000-0003-1169-7870
André T LopesUK Dementia Research Institute at University College London, London, UK.
Skye StuartUK Dementia Research Institute at University College London, London, UK.
Samantha De La-RocqueUK Dementia Research Institute at University College London, London, UK.
Maria Giuseppa CasoInstitute of Neuroscience, CNR, Milan, Italy.
Ian J WhiteLaboratory for Molecular Cell Biology, University College London, London, UK.
Samuel S HarrisUK Dementia Research Institute at University College London, London, UK.
Marc Aurel BuscheUK Dementia Research Institute at University College London, London, UK.ORCID http://orcid.org/0000-0002-4416-7553
Giampietro SchiavoUK Dementia Research Institute at University College London, London, UK. giampietro.schiavo@ucl.ac.uk.ORCID http://orcid.org/0000-0002-4319-8745

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impairments in axonal transport have been implicated in the pathogenesis of tauopathies, including frontotemporal dementia and Alzheimer's disease, yet the underlying mechanisms and reversibility of these deficits are largely unknown. In particular, the impacts of tau mutations, phosphorylation and aggregation on axonal transport in vivo remain controversial. By using two-photon imaging of axonal transport of BDNF granules in the mouse cortex, we reveal that deficits in axonal transport arise in vivo at early stages of tau pathology, preceding tangle formation and neuronal death. Mechanistically, these impairments are caused by the enlargement of tau envelopes on microtubules, which act as functional barriers for transport. Crucially, these deficits are reversed by inhibiting MAPK p38α. Together, our work demonstrates that tau pathology causes reversible deficits in axonal transport in vivo, posing the basis for pharmacological interventions to restore the physiological flux of axonal organelles and cargoes in tauopathies.

Indexed as

Axonal TransportBrain-Derived Neurotrophic FactorMitogen-Activated Protein Kinase 14tau ProteinsAlzheimer DiseaseAnimalsBrainCell DeathDoxycyclineFrontotemporal DementiaMiceMice, Inbred C57BLMicrotubulesMitogen-Activated Protein Kinase 11NeuroimagingNeuronsBdnf protein, mouseBrain-Derived Neurotrophic FactorDoxycyclineMapt protein, mouseMitogen-Activated Protein Kinase 11Mitogen-Activated Protein Kinase 14tau Proteins

Identifiers

PMID42243402
PMCPMC13246509

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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.