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NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review
Yujia Lu, Lin Cheng, Yinyi Xiong, Chunyan Huang, Ziying Liu, Chunxiao Shen, Huaying Wang, Yuemin Qiu et al.. CNS Neuroscience & Therapeutics, 2025-05-01
Topic: Brain proteins, microglia and lab models
The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β. Moreover, it exacerbates vascular dementia by producing IL-18, IL-1β, and the N-terminal fragment of GSDMD, which also contributes to neuronal cell death. Thus, blocking the NLRP3 inflammasome pathway presents a new therapeutic strategy for treating vascular dementia, thereby delaying or curing the disease more effectively and mitigating adverse effects. This review explores the role and mechanisms of the NLRP3 inflammasome in vascular dementia, summarizing current research and therapeutic strategies. Investigating the activation of the NLRP3 inflammasome can reveal the pathogenesis of vascular dementia from a new perspective and propose innovative preventive and treatment strategies.
Key findings
- The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β.
- Moreover, it exacerbates vascular dementia by producing IL-18, IL-1β, and the N-terminal fragment of GSDMD, which also contributes to neuronal cell death.
- Thus, blocking the NLRP3 inflammasome pathway presents a new therapeutic strategy for treating vascular dementia, thereby delaying or curing the disease more effectively and mitigating adverse effects.
- This review explores the role and mechanisms of the NLRP3 inflammasome in vascular dementia, summarizing current research and therapeutic strategies.
- Investigating the activation of the NLRP3 inflammasome can reveal the pathogenesis of vascular dementia from a new perspective and propose innovative preventive and treatment strategies.
Why it matters
This review describes how the NLRP3 inflammasome pathway destroys neuronal cells through IL-18, IL-1β and the N-terminal fragment of GSDMD in vascular dementia, and proposes that blocking this pathway is a new therapeutic strategy. The proposed treatment target is for vascular dementia, not Alzheimer's disease, and no clinical trial results are reported.
Study details
- Evidence strengthLow
How this study scored 38/100
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 (CNS Neuroscience & Therapeutics) |
| Journal's citation record | 1 / 4 | CNS Neuroscience & Therapeutics: journal h-index 120 (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 | 2 / 7 | Cited 12 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 3.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Xiaorong Zhang: h-index 5 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Jiujiang University: institution h-index 109 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40326096) |
| Free to read | 2 / 2 | Free to read |
| Total | 38 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/cns.70403
- PubMed: 40326096
- Original source →
- Free full text: CNS Neuroscience & Therapeutics →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Lu, Y., Cheng, L., Xiong, Y., Huang, C., Liu, Z., Shen, C., et al. (2025). NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review. CNS Neuroscience & Therapeutics. https://doi.org/10.1111/cns.70403
Vancouver
Lu Y, Cheng L, Xiong Y, Huang C, Liu Z, Shen C, et al. NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review. CNS Neuroscience & Therapeutics. 2025. doi:10.1111/cns.70403. PMID: 40326096.
BibTeX
@article{lu2025-40326096,
author = {Lu, Yujia and Cheng, Lin and Xiong, Yinyi and Huang, Chunyan and Liu, Ziying and Shen, Chunxiao and Wang, Huaying and Qiu, Yuemin and others},
title = {{NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review}},
journal = {CNS Neuroscience \& Therapeutics},
year = {2025},
doi = {10.1111/cns.70403},
pmid = {40326096},
url = {https://doi.org/10.1111/cns.70403}
}
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