ReviewBiomolecules2025
Inflammasome-Mediated Neuroinflammation: A Key Driver in Alzheimer's Disease Pathogenesis.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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Who cites it
23 citing papers in PubMed.
- Effects of a Combined Vitamin DNutrients · 2026Trial
- Plant-derived phytochemicals for Alzheimer's disease: mechanisms of action, experimental evidence, and therapeutic perspectives.Journal of natural medicines · 2026Review
- Nanomedicine targeting neuroinflammatory pathways in Alzheimer's disease: a new frontier in inflammopharmacology.Inflammopharmacology · 2026Review
- SOX9 knockdown alleviates Aβ1‑42‑induced neuroinflammation by regulating microglial polarization via inactivation of the ASK1/JNK signaling pathway.Journal of molecular histology · 2026Article
- Forced treadmill running and ladder climbing physical activity attenuates cognitive decline and protein aggregates in aged 3xTg-AD mice.Molecular brain · 2026Article
- Regulatory Effects of the PDE8B Inhibitor PF-04957325 on Cognitive Impairment and Neuroinflammation in Aβ-Induced Alzheimer's Disease Mouse Models.Neurochemical research · 2026Article
- Roles of Lcn2 and neuroinflammation in a scopolamine-induced cognitive impairment animal model: implication of the NLRP3 inflammasome pathway.Genes & genomics · 2026Article
- Review
- The Immune-Chemokine Axis in Alzheimer's Disease: Roles of Adaptive Immune System in Neuroinflammation and Disease Progression.Biomolecules · 2026Review
- LLPS Inflammasome Metabo-Proteostatic Failure Axis in AD: Mechanistic and Translational Insights.Molecular neurobiology · 2026Review
- Review
- Antiaging Properties of the Klotho Protein.Cells · 2026Review
- Mesenchymal Stem Cell-Based Therapies Applied in Neurological Diseases: A Systematic Review.Biomedicines · 2026Review
- Alzheimer's Disease as a Disorder of Neuroimmune Dysregulation.Neurology international · 2026Review
- From Traumatic Brain Injury to Alzheimer's Disease: Multilevel Biomechanical, Neurovascular, and Molecular Mechanisms with Emerging Therapeutic Directions.International journal of molecular sciences · 2026Review
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Intermittent Fasting Potentiates Aerobic Exercise to Reduce Hippocampal Amyloid Burden and Oxidative Stress via Suppression of NF-κB/NLRP3 Signaling in an Aβ-Injected Rat Model.Oxidative medicine and cellular longevity · 2026Article
- Accelerated biological aging: the role of chronic inflammation, weathering and novel therapeutic strategies.Frontiers in aging · 2026Review
- The inhibition of the Aβ-ASC interaction site suppresses β-amyloid aggregation and cytotoxicity.Frontiers in immunology · 2026Article
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder predominantly affecting the elderly, characterized by memory loss, cognitive decline, and functional impairment. While hallmark pathological features include extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein, increasing evidence points to chronic neuroinflammation as a key driver of disease progression. Among inflammatory mechanisms, the activation of the NLRP3 (nucleotide-binding domain, leucine-rich repeat, and pyrin domain-containing protein 3) inflammasome in microglia plays a pivotal role by amplifying neuroinflammatory cascades, exacerbating synaptic dysfunction, and accelerating neuronal loss. This review examines the molecular underpinnings of AD with a focus on NLRP3 inflammasome-mediated neuroinflammation, detailing the crosstalk between Aβ, tau pathology, and innate immune responses. Finally, we highlight emerging therapeutic strategies targeting NLRP3 inflammasome activation as promising avenues for mitigating neuroinflammation and slowing AD progression.
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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 OpenQuestion graph.