ReviewFrontiers in immunology2025
NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Diagnostic Value of Inflammatory Biomarkers in Differentiating Vascular Dementia From Alzheimer's Disease: A Systematic Review and Meta-Analysis.Brain and behavior · 2026Pooled it
- Effects of a Combined Vitamin DNutrients · 2026Trial
- Increased expression of inflammasome signaling genes and proteins in selective brain regions in the intermediate stage of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
- Article
- Molecular Regulation of Pyroptosis in Alzheimer's Disease: Linking Neuroinflammation, Cell Death, and Therapeutic Targeting.Molecular neurobiology · 2026Review
- Microglial checkpoint collapse in Alzheimer's disease: a tri-axial framework for biomarker-informed neuroimmune therapy.Journal of neuroinflammation · 2026Review
- Targeting inflammaging in Alzheimer's disease: molecular pathways and emerging pharmacotherapies.Inflammopharmacology · 2026Review
- CRP Is a Key Indicator of Rheumatoid Arthritis-Associated Vascular Injury and Neurodegeneration.International journal of molecular sciences · 2026Review
- Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026Review
- SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice.Redox biology · 2026Article
- Reimagining GSK-3β Therapeutics in Alzheimer's Disease: From Inhibition to Activity Normalization and Targeted Degradation.Journal of molecular neuroscience : MN · 2026Review
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Antiaging Properties of the Klotho Protein.Cells · 2026Review
- Modulation of the Kynurenine Pathway: A New Approach for Treating Neurodegeneration.Life (Basel, Switzerland) · 2026Review
- Radiation-Induced Neurodegeneration.Biomedicines · 2026Review
- Lipid metabolic regulation of neuroinflammation in Alzheimer's disease.Frontiers in immunology · 2026Review
- Infection, vaccination and risk of dementia: a proposed immunological model.Frontiers in immunology · 2026Review
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
- The regulatory mechanism of NLRP3 inflammasome in the "immune paralytic-overactivation" imbalance in sepsis: the latest progress from molecular signaling to clinical translation.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and neuroinflammation, with no definitive cure currently available. The NLRP3 inflammasome, a key mediator of neuroinflammation, has emerged as a critical player in AD pathogenesis, contributing to the accumulation of β-amyloid (Aβ) plaques, tau hyperphosphorylation, and neuronal damage. This review explores the mechanisms by which the NLRP3 inflammasome is activated in AD, including its interactions with Aβ, tau, reactive oxygen species (ROS), and pyroptosis. Additionally, it highlights the role of the ubiquitin system, ion channels, autophagy, and gut microbiota in regulating NLRP3 activation. Therapeutic strategies targeting the NLRP3 inflammasome, such as IL-1β inhibitors, natural compounds, and novel small molecules, are discussed as promising approaches to mitigate neuroinflammation and slow AD progression. This review underscores the potential of NLRP3 inflammasome inhibition as a therapeutic avenue for AD.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.