ReviewCNS neuroscience & therapeutics2025
NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A Comprehensive Review.
Review in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- A Study on the Effects of Intranasally Administered Liquid Crystalline Nanoparticles Loaded with Salvianolic Acid B in Vascular Dementia.Molecular neurobiology · 2026Article
- Pathological Roles of Astrocytes in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2026Review
- The enigma of vascular dementia: current state and emerging perspectives.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Elevated serum inflammasome adaptor protein ASC is associated with white matter hyperintensities in vascular cognitive impairment.Brain communications · 2026Article
- Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer.Iranian journal of basic medical sciences · 2026Review
- Piracetam attenuates oxidative stress and inflammation-induced neuronal cell death in rats with vascular dementia potentially via the activation of the AMPK/SIRT-1/Nrf-2 signaling pathway.Metabolic brain disease · 2025Article
- Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundVascular dementia, the second most common type of dementia globally after Alzheimer's disease, is associated with neuroinflammation. Activation of the NLRP3 inflammasome, an important pattern recognition receptor in human innate immunity, plays a key role in the pathogenesis of vascular dementia.
resultsThe 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.
conclusionsThis 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.
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Registered trials
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