ReviewFrontiers in neurology2020
The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease.
Review in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses 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
133 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.Molecular and cellular biochemistry · 2025Pooled it
- A role of NLRP3 and MMP9 in migraine progression: a systematic review of translational study.Frontiers in neurology · 2024Pooled it
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- Exercise-Mediated Modulation of the NLRP3 Inflammasome in Aging and Neurodegenerative Diseases: Mechanisms, Microglial Crosstalk, and Translational Perspectives.Molecular neurobiology · 2026Review
- Microglial synaptic pruning in early Alzheimer's disease: emerging roles of the IL-1β-NLRP3 axis.Inflammopharmacology · 2026Review
- Retinitis pigmentosa elicits neurodegeneration within the visual pathway in REEP6 knockout mice.Neural regeneration research · 2026Article
- Total Saponins of Panax Notoginseng Leaves Modulate the "Microglial-NLRP3/Caspase-1" Axis associated with Gut Microbial/SCFAs Alterations: Correlative Insights into Cognitive Improvement in Senescence.Molecular neurobiology · 2026Article
- Decoding neuroinflammation: the critical role of NLRP3 inflammasome in Alzheimer's disease.Inflammopharmacology · 2026Review
- Review
- LLPS Inflammasome Metabo-Proteostatic Failure Axis in AD: Mechanistic and Translational Insights.Molecular neurobiology · 2026Review
- Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 2026Review
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026Review
- Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases.Apoptosis : an international journal on programmed cell death · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Ganaxolone as a promising therapeutic agent for Alzheimer's disease: signaling pathways and mechanistic insights-a narrative review.Inflammopharmacology · 2026Review
- The Immuno-Glial Connectome in Alzheimer's Disease: Integrating Central and Peripheral Inflammatory Networks.Cellular and molecular neurobiology · 2026Review
- Early-life cognitive intervention preserves brain function in aged TgF344-AD rats with sex-specific effects.iScience · 2026Article
- Oxidative Stress and Lysosomal Dysfunction in Neurodegenerative Diseases: Underlying Mechanisms and Nanotherapeutic Targeting Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Alzheimer's disease (AD) is the most prevalent form of late-onset dementia. AD affects the health of millions of people in the United States and worldwide. Currently, there are no approved therapies that can halt or reverse the clinical progression of AD. Traditionally, AD is characterized first by the appearance of amyloid-β (Aβ) plaques followed by the formation of intraneuronal neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (p-tau). These lesions are linked to synapse loss and eventual cognitive impairment. Additionally, microgliosis is consistently found in regions of the brain with AD pathology. The role of microglia in AD onset and progression remains unclear. Several recent reports indicate that the assembly of the multi-protein complex known as the NOD, LRR, and pyrin-domain containing 3 (Nlrp3) inflammasome by microglia results in apoptosis spec-like protein containing a CARD (Asc) spec formation, which then nucleates new Aβ plaques, thus amplifying Aβ-associated pathology. NFTs can also activate the Nlrp3 inflammasome leading to enhanced tau-associated pathology. Here, we will review the role of microglia and the activation of the inflammasome in the innate immune response to AD.
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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.