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42/100

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Plain-language summary

AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration. Furthermore, TAU overexpression induced pyroptosis in both mouse models, and GSDMD protein levels increased alongside reactive microglial morphology. Our data supports that TAU-induced neuroinflammation correlated with synaptic plasticity impairment. GSDMD deficiency significantly reduced pyroptosis-related markers associated to TAU, but unexpectedly worsened synaptic plasticity deficits, suggesting GSDMD may play a dual role in inflammation and synaptic function. Finally, we showed that DMF treatment suppressed pyroptosis gene expression, reduced GSDMD levels, and alleviated neuroinflammation, correlating with improved synaptic marker expression. Our findings demonstrate that TAU-induced pyroptosis contributes to neuroinflammation and synaptic dysfunction. While GSDMD inhibition mitigates inflammation, its absence exacerbates synaptic impairment, highlighting its complex role in tauopathies. Our results indicate that DMF treatment could offer a promising therapeutic avenue to modulate pyroptosis and neuroinflammation, and restore synaptic integrity in tauopathies.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Silva-Llanes, I., Smith, L. A., Abdelkader-Guillén, A., Jiménez-Villegas, J., Sarrió, D., Gema, M.-B., et al. (2026). GASDERMIN D-mediated pyroptosis as a therapeutic target in TAU-dependent frontotemporal dementia mouse model. Journal of Biomedical Science. https://doi.org/10.1186/s12929-025-01210-1

Vancouver

Silva-Llanes I, Smith LA, Abdelkader-Guillén A, Jiménez-Villegas J, Sarrió D, Gema M.-B, et al. GASDERMIN D-mediated pyroptosis as a therapeutic target in TAU-dependent frontotemporal dementia mouse model. Journal of Biomedical Science. 2026. doi:10.1186/s12929-025-01210-1. PMID: 41486173.

BibTeX

@article{silvallanes2026-41486173,
  author  = {Silva-Llanes, Ignacio and Smith, Lilia A. and Abdelkader-Guillén, Aaron and Jiménez-Villegas, José and Sarrió, David and Gema, Moreno-Bueno and Lastres‐Becker, Isabel},
  title   = {{GASDERMIN D-mediated pyroptosis as a therapeutic target in TAU-dependent frontotemporal dementia mouse model}},
  journal = {Journal of Biomedical Science},
  year    = {2026},
  doi     = {10.1186/s12929-025-01210-1},
  pmid    = {41486173},
  url     = {https://doi.org/10.1186/s12929-025-01210-1}
}

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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration.
Furthermore, TAU overexpression induced pyroptosis in both mouse models, and GSDMD protein levels increased alongside reactive microglial morphology.
Our data supports that TAU-induced neuroinflammation correlated with synaptic plasticity impairment.
GSDMD deficiency significantly reduced pyroptosis-related markers associated to TAU, but unexpectedly worsened synaptic plasticity deficits, suggesting GSDMD may play a dual role in inflammation and synaptic function.
Finally, we showed that DMF treatment suppressed pyroptosis gene expression, reduced GSDMD levels, and alleviated neuroinflammation, correlating with improved synaptic marker expression.

Why it matters

In mouse models, TAU overexpression induced pyroptosis and neuroinflammation, and while GSDMD deficiency reduced pyroptosis-related markers it unexpectedly worsened synaptic plasticity deficits; DMF treatment suppressed pyroptosis gene expression, reduced GSDMD levels and alleviated neuroinflammation. The authors suggest DMF could be a therapeutic avenue in tauopathies, but this is animal and laboratory work, not a proven treatment, cure or prevention.

Study details

Evidence strengthLow

How this study scored 42/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of Biomedical Science)
Journal's citation record	2 / 4	Journal of Biomedical Science: journal h-index 151 (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	5 / 5	2026 — within 1 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	Laboratory or animal study (title names “mouse”) — scores zero
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	2 / 7	Cited 6 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	3.0 citations a year over 2 year(s) since 2026
Impact for its field and year	4 / 6	Cited 11.6× 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	1 / 4	Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Isabel Lastres‐Becker: h-index 40 (OpenAlex, whole career)
Institution's track record	0 / 3	Instituto de Salud Carlos III: institution h-index 649 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 8 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41486173)
Free to read	2 / 2	Free to read
Total	42 / 100	—

What each of these 20 components measures, and what this score is not →

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