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Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential
Elizabeth R. Dellar, Lara Nikel, Stephanie L. Fowler, Björn Friedhelm Vahsen, Ruxandra Dafinca, Emily Feneberg, Kevin Talbot, Martin R. Turner et al.. Molecular Neurodegeneration, 2025-06-10
Topic: Brain proteins, microglia and lab models
Extracellular vesicles (EVs) are membrane-enclosed nanoparticles released by most cell types, and from multiple sub-cellular compartments. They carry a range of cargo biomolecules, including protein and RNA that reflect the type and status of their cell of origin. EVs are associated with the 43 kDa trans-active response DNA binding protein (TDP-43), aggregates of which are a key pathological feature across the spectrum of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other TDP-43 proteinopathies. The secretion of TDP-43 via EVs may have beneficial effects through the cellular clearance of aggregated protein, or detrimental effects via the intercellular spread of templated TDP-43 aggregation. This review examines evidence for the association of TDP-43 with EVs in post mortem tissue, in vitro models and human biofluids, and discusses evidence for EV TDP-43 involvement in pathogenesis via clearance or ‘seeding’ processes. We further discuss the potential for use of EVs in biomarker development, through analysis of TDP-43 or alternative protein and RNA cargoes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Dellar, E. R., Nikel, L., Fowler, S. L., Vahsen, B. F., Dafinca, R., Feneberg, E., et al. (2025). Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-025-00859-4
Vancouver
Dellar ER, Nikel L, Fowler SL, Vahsen BF, Dafinca R, Feneberg E, et al. Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-025-00859-4. PMID: 40495245.
BibTeX
@article{dellar2025-40495245,
author = {Dellar, Elizabeth R. and Nikel, Lara and Fowler, Stephanie L. and Vahsen, Björn Friedhelm and Dafinca, Ruxandra and Feneberg, Emily and Talbot, Kevin and Turner, Martin R. and others},
title = {{Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential}},
journal = {Molecular Neurodegeneration},
year = {2025},
doi = {10.1186/s13024-025-00859-4},
pmid = {40495245},
url = {https://doi.org/10.1186/s13024-025-00859-4}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- EVs are associated with the 43 kDa trans-active response DNA binding protein (TDP-43), aggregates of which are a key pathological feature across the spectrum of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other TDP-43 proteinopathies.
Why it matters
This review examines evidence that TDP-43 is associated with extracellular vesicles, which may either help clear aggregated protein or spread it between cells. It discusses potential use of extracellular vesicles as biomarkers, but reports no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular Neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 17 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 4 / 6 | Cited 9.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Alexander G. Thompson: h-index 21 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Oxford: institution h-index 2,205 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40495245) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-025-00859-4
- PubMed: 40495245
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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