Evidence map›Paper›PMID 41631437›Full record

ArticleDisease models & mechanisms2026

Drosophila wing is a high-throughput and versatile screening tool for Tau-mediated disease mechanisms and drug discovery.

Miguel Ramirez-Moreno, Amber S Cooper, Tianshun Lian, Jie Liu, Seyedehleila Abtahi, Efthimios M C Skoulakis, Lovesha Sivanantharajah, Douglas Watt Allan, Amritpal Mudher

Abstract read
In one paragraph

Article in Disease models & mechanisms, 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.

Miguel Ramirez-MorenoSchool of Biological Sciences, University of Southampton, Southampton SO17 1BJ, UK.ORCID 0000-0003-1559-8976
Amber S CooperSchool of Biological Sciences, University of Southampton, Southampton SO17 1BJ, UK.ORCID 0000-0003-2525-0148
Tianshun LianDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver V6T 1Z3, Canada.
Jie LiuDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver V6T 1Z3, Canada.
Seyedehleila AbtahiDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver V6T 1Z3, Canada.ORCID 0000-0003-3672-3705
Efthimios M C SkoulakisInstitute for Fundamental Biomedical Research, Biomedical Sciences Research Centre "Alexander Fleming", Vari 16672, Greece.ORCID 0000-0001-5113-6192
Lovesha SivanantharajahSchool of Biological Sciences, Bangor University, Bangor LL57 2UW, UK.ORCID 0009-0009-5160-2697
Douglas Watt AllanDepartment of Cellular and Physiological Sciences, Life Science Institute, University of British Columbia, Vancouver V6T 1Z3, Canada.ORCID 0000-0002-3488-8365
Amritpal MudherSchool of Biological Sciences, University of Southampton, Southampton SO17 1BJ, UK.ORCID 0000-0002-0880-1107

Funding

Alzheimer Society 2020Alzheimer Society ALZSOCCAAlzheimer Society of Canada ALZSOCCAAlzheimer's Society 575, AS-PG-21-033Art Libraries Society UK and Ireland AS-PG-21-033 (575)Gerald Kerkut Charitable TrustUBC Centre for Brain Health 2023 DMCBH Alzheimer Disease Research GrantUniversity of British Columbia UBCCBH 2023University of Southampton
6 · The paper itself

Abstract

Tau protein contributes to microtubule stability, which is disrupted in Alzheimer's disease and other tauopathies. In these diseases, Tau molecules become hyperphosphorylated, misfolded and aggregated, propagating pathology across the brain. Studies dissecting disease mechanisms or screening disease-modifying therapies rely on animal models that unveil pathogenic events in vivo but also take several weeks or months to complete. Here, we describe a versatile experimental paradigm that yields results in days and yet offers all the advantages of a genetically tractable in vivo system: the Drosophila wing. Mimicking neurotoxicity, human Tau expression caused cell death in Drosophila wing disc, leading to quantifiable phenotypes in the adult wing. The neuroprotective peptide NAPVSIPQ ameliorated Tau toxicity in this system, validating it as a cost-effective drug-screening tool. Phenocopying adult neurons, Tau toxicity in the wing disc was exacerbated by simulating hyperphosphorylation and prevented by suppressing aggregation. Additionally, we showed that the wing disc can dissect disease mechanisms that underpin clinically relevant Tau variants. Thus, the Drosophila wing offers an in vivo experimental paradigm for fast and efficient exploration of disease mechanism and screening.

Indexed as

Drosophila melanogasterDrug DiscoveryHigh-Throughput Screening AssaysTauopathiestau ProteinsWings, AnimalAnimalsDisease Models, AnimalDrosophila ProteinsHumansImaginal DiscsNeuronsPeptidesPhenotypePhosphorylationDrosophila ProteinsPeptidestau ProteinsDrosophilaNeurodegenerationTauTauopathiesWingWing disc

Identifiers

PMID41631437
PMCPMC12994453

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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.