Evidence map›Paper›PMID 41205178›Full record

ArticleCell reports2025

Therapeutic VEGFC treatment provides protection against traumatic-brain-injury-driven tauopathy pathogenesis.

Ana Royo Marco, Katherine R Bruch, Maureen N Cowan, Julia G Dill, Katelyn A Moore, Ashley C Bolte, John R Lukens

Abstract read
In one paragraph

Article in Cell reports, 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. Review
  2. Review
  3. Review
  4. 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

7 authors.

Ana Royo MarcoCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA; Department of Microbiology, Immunology and Cancer Biology, University of Virginia (UVA), Charlottesville, VA 22908, USA. Electronic address: ar5wz@virginia.edu.
Katherine R BruchCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA.
Maureen N CowanCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA.
Julia G DillCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA.
Katelyn A MooreCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA.
Ashley C BolteCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA.
John R LukensCenter for Brain Immunology and Glia (BIG), Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA 22908, USA. Electronic address: jrl7n@virginia.edu.

Funding

Inflammasome activation and lymphatic dysfunction in traumatic brain injuryR01NS106383 · NINDS · UNIVERSITY OF VIRGINIA · PI LUKENS, JOHN R · 2018 to 2022
$1.8M
NINDS NIH HHS R01 NS106383
6 · The paper itself

Abstract

Traumatic brain injury (TBI) increases one's risk of developing Alzheimer's disease and tauopathy. Yet, the mechanisms linking TBI to neurodegenerative disease remain poorly defined. Mounting recent evidence indicates that defects in brain lymphatic drainage contribute to multiple neurodegenerative diseases. Here, we investigated whether promoting brain lymphatic drainage recuperation following TBI via treatment with the lymphangiogenic factor vessel endothelial growth factor C (VEGFC) mitigates the ability of TBI to exacerbate tauopathy. In this study, we show that a single mild TBI leads to worsened neuropathology, brain macrophage activation, and neurodegeneration in the PS19 mouse model of tauopathy. Moreover, we find that viral-vector-based delivery of VEGFC into the meningeal compartment 24 h post-TBI ameliorates tau-mediated neurodegenerative disease pathogenesis. Findings from these studies offer new insights into how TBI leads to the development of tauopathy later in life and suggest that VEGFC-based treatments might offer a therapeutic strategy to limit tauopathy after sustaining a head injury.

Indexed as

Brain Injuries, TraumaticTauopathiesVascular Endothelial Growth Factor CAnimalsBrainDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, Transgenictau Proteinstau ProteinsVascular Endothelial Growth Factor CAlzheimer's Diseasebrain lymphaticsCP: neurosciencemicroglianeurodegenerative diseasetauopathytraumatic brain injuryVegfc

Identifiers

PMID41205178
PMCPMC12743485

What OpenQuestion holds

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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.