Evidence map›Paper›PMID 40144670›Full record

ArticleFrontiers in pharmacology2025

Exosomes enriched with miR-124-3p show therapeutic potential in a new microfluidic triculture model that recapitulates neuron-glia crosstalk in Alzheimer's disease.

Artemizia Évora, Gonçalo Garcia, Ana Rubi, Eleonora De Vitis, Ana Teresa Matos, Ana Rita Vaz, Francesca Gervaso, Giuseppe Gigli, Alessandro Polini, Dora Brites

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  15. Extracellular vesicle-based therapies for neurodegenerative diseases.NeuroImmune pharmacology and therapeutics · 2025
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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

10 authors.

Artemizia Évora *Neuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Gonçalo Garcia *Neuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Ana RubiNeuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Eleonora De VitisInstitute of Nanotechnology, National Research Council (CNR Nanotec), Lecce, Italy.
Ana Teresa MatosNeuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Ana Rita VazNeuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Francesca GervasoInstitute of Nanotechnology, National Research Council (CNR Nanotec), Lecce, Italy.
Giuseppe GigliInstitute of Nanotechnology, National Research Council (CNR Nanotec), Lecce, Italy.
Alessandro PoliniInstitute of Nanotechnology, National Research Council (CNR Nanotec), Lecce, Italy.
Dora BritesNeuroinflammation, Signaling and Neuroregeneration, Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alzheimer's disease (AD), a complex neurodegenerative disease associated with ageing, is the leading cause of dementia. Few people with early AD are eligible for the novel Food and Drug Administration (FDA)-approved drug treatments. Accordingly, new tools and early diagnosis markers are required to predict subtypes, individual stages, and the most suitable personalized treatment. We previously demonstrated that the regulation of microRNA (miR)-124 is crucial for proper neuronal function and microglia reshaping in human AD cell models. Objective: The aim of this study was to develop an efficient miR-124-3p-loaded exosome strategy and validate its therapeutic potential in using a multi-compartment microfluidic device of neuron-glia that recapitulates age-AD pathological features. Methods and results: Using cortical microglia from mouse pups, separated from glial mixed cultures and maintained for 2 days Conclusion: To the best of our knowledge, this is the first study supporting the neuro- and immunoprotective properties of miR-124-engineered exosomes in a microfluidic triculture platform, recapitulating age-related susceptibility to AD. Our system offers potential to develop personalized medicines in AD patient subtypes.

Indexed as

Alzheimer’s disease modellinghuman neural triculturesmicrofluidic systemmiR-124-3p mimicmiRNA-engineered exosomesneuron-glia communicationSH-SY5Y cells transfected with APP695

Identifiers

PMID40144670
PMCPMC11936931

What Socratic 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 Socratic graph.