ArticleAging cell2022
New lessons on TDP-43 from old N. furzeri killifish.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Engulfment by brain macrophages in a short-lived vertebrate.bioRxiv : the preprint server for biology · 2026Article
- Altered translation elongation contributes to key hallmarks of aging in the killifish brain.Science (New York, N.Y.) · 2025Article
- Aging and diet alter the protein ubiquitylation landscape in the mouse brain.Nature communications · 2025Article
- Early-life growth and cellular heterogeneity in the short-lived African turquoise killifish telencephalon.Biology open · 2025Article
- A short-lived fish with long-lasting effects: hallmarks of aging inFrontiers in aging · 2025Review
- Age-related dysregulation of the retinal transcriptome in African turquoise killifish.Aging cell · 2024Article
- Age-related dysregulation of the retinal transcriptome in African turquoise killifish.bioRxiv : the preprint server for biology · 2024Article
- Impaired biogenesis of basic proteins impacts multiple hallmarks of the aging brain.bioRxiv : the preprint server for biology · 2024Article
- Article
- New lessons on TDP-43 from old N. furzeri killifish.Aging cell · 2022Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frontotemporal dementia and amyotrophic lateral sclerosis are fatal and incurable neurodegenerative diseases linked to the pathological aggregation of the TDP-43 protein. This is an essential DNA/RNA-binding protein involved in transcription regulation, pre-RNA processing, and RNA transport. Having suitable animal models to study the mechanisms of TDP-43 aggregation is crucial to develop treatments against disease. We have previously demonstrated that the killifish Nothobranchius furzeri offers the advantage of being the shortest-lived vertebrate with a clear aging phenotype. Here, we show that the two N. furzeri paralogs of TDP-43 share high sequence homology with the human protein and recapitulate its cellular and biophysical behavior. During aging, N. furzeri TDP-43 spontaneously forms insoluble intracellular aggregates with amyloid characteristics and colocalizes with stress granules. Our results propose this organism as a valuable new model of TDP-43-related pathologies making it a powerful tool for the study of disease mechanism.
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