Evidence map›Paper›PMID 38721655›Full record

ArticleDisease models & mechanisms2024

An ALS-associated mutation dysregulates microglia-derived extracellular microRNAs in a sex-specific manner.

Eleni Christoforidou, Libby Moody, Greig Joilin, Fabio A Simoes, David Gordon, Kevin Talbot, Majid Hafezparast

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2024. 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. Review
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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

7 authors.

Eleni ChristoforidouSussex Neuroscience, School of Life Sciences, University of Sussex, Brighton, BN1 9QG, UK.ORCID 0000-0002-9352-4908
Libby MoodySussex Neuroscience, School of Life Sciences, University of Sussex, Brighton, BN1 9QG, UK.
Greig JoilinSussex Neuroscience, School of Life Sciences, University of Sussex, Brighton, BN1 9QG, UK.ORCID 0000-0001-5827-6382
Fabio A SimoesSussex Neuroscience, School of Life Sciences, University of Sussex, Brighton, BN1 9QG, UK.ORCID 0000-0001-7630-0091
David GordonNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK.
Kevin TalbotNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, UK.ORCID 0000-0001-5490-1697
Majid HafezparastSussex Neuroscience, School of Life Sciences, University of Sussex, Brighton, BN1 9QG, UK.ORCID 0000-0002-5262-7150

Funding

Motor Neurone Disease Association Hafezparast/Apr21/880-791My Name'5 Doddie Foundation DOD/14/30-PF12794University of Sussex
6 · The paper itself

Abstract

Evidence suggests the presence of microglial activation and microRNA (miRNA) dysregulation in amyotrophic lateral sclerosis (ALS), the most common form of adult motor neuron disease. However, few studies have investigated whether the miRNA dysregulation originates from microglia. Furthermore, TDP-43 (encoded by TARDBP), involved in miRNA biogenesis, aggregates in tissues of ∼98% of ALS cases. Thus, this study aimed to determine whether expression of the ALS-linked TDP-43M337V mutation in a transgenic mouse model dysregulates microglia-derived miRNAs. RNA sequencing identified several dysregulated miRNAs released by transgenic microglia and a differential miRNA release by lipopolysaccharide-stimulated microglia, which was more pronounced in cells from female mice. We validated the downregulation of three candidate miRNAs, namely, miR-16-5p, miR-99a-5p and miR-191-5p, by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and identified their predicted targets, which primarily include genes involved in neuronal development and function. These results suggest that altered TDP-43 function leads to changes in the miRNA population released by microglia, which may in turn be a source of the miRNA dysregulation observed in the disease. This has important implications for the role of neuroinflammation in ALS pathology and could provide potential therapeutic targets.

Indexed as

Amyotrophic Lateral SclerosisMice, TransgenicMicrogliaMicroRNAsMutationSex CharacteristicsAnimalsDNA-Binding ProteinsExtracellular SpaceFemaleGene Expression RegulationHumansLipopolysaccharidesMaleMiceDNA-Binding ProteinsLipopolysaccharidesMicroRNAsAmyotrophic lateral sclerosisMicrogliaMicroRNAMotor neuron diseaseTDP-43

Identifiers

PMID38721655
PMCPMC11152562

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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.