ReviewSeminars in immunopathology2015
β-amyloid, microglia, and the inflammasome in Alzheimer's disease.
Review in Seminars in immunopathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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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.
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Who cites it
110 citing papers in PubMed, 179 citations in OpenAlex.
- Microglial synaptic pruning in early Alzheimer's disease: emerging roles of the IL-1β-NLRP3 axis.Inflammopharmacology · 2026Review
- Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.iScience · 2026Article
- Review
- Lobar versus sub-lobar resection for clinical stage IA (≤ 2 cm) lung neuroendocrine tumor with spread through air spaces: a multi-center study.Updates in surgery · 2025Article
- Ultrasonic disruption of circulating amyloid β aggregates via phase-change peptide nanoemulsions.Biomaterials · 2025Article
- Role of NLRP3 Inflammasome in Chronic Pain and Alzheimer's Disease-A Review.Journal of biochemical and molecular toxicology · 2025Review
- Glycolytic reprogramming during microglial polarization in neurological diseases.Frontiers in immunology · 2025Review
- Causal Relationships Between Neuropathic Pain and Alzheimer's Disease: A Multi-Omics Mendelian Randomization Study with Exploratory Evidence of a Potential Protective Role of Diabetic Neuropathy.Journal of pain research · 2025Article
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Variant-to-function mapping of late-onset Alzheimer's disease GWAS signals in human microglial cell models implicatesbioRxiv : the preprint server for biology · 2024Article
- MSC-Derived Extracellular Vesicles Alleviate NLRP3/GSDMD-Mediated Neuroinflammation in Mouse Model of Sporadic Alzheimer's Disease.Molecular neurobiology · 2024Article
- Gender differences in Alzheimer's may be associated with TLR4-LYN expression in damage associated microglia and neuronal phagocytosis.Journal of cellular physiology · 2024Article
- A common molecular and cellular pathway in developing Alzheimer and cancer.Biochemistry and biophysics reports · 2024Review
- Understanding immune microenvironment alterations in the brain to improve the diagnosis and treatment of diverse brain diseases.Cell communication and signaling : CCS · 2024Review
- Hotspots and trends of microglia in Alzheimer's disease: a bibliometric analysis during 2000-2022.European journal of medical research · 2024Article
- Interactions of Cellular Energetic Gene Clusters in the Alzheimer's Mouse Brain.Molecular neurobiology · 2024Article
- Correlation between Blood Monocytes and CSF Tau in Alzheimer's Disease: The Effect of Gender and Cognitive Decline.NeuroSci · 2023Article
- N-Acetylcysteine Amide against Aβ-Induced Alzheimer's-like Pathology in Rats.International journal of molecular sciences · 2023Article
- Extracellular tau stimulates phagocytosis of living neurons by activated microglia via Toll-like 4 receptor-NLRP3 inflammasome-caspase-1 signalling axis.Scientific reports · 2023Article
- Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
There is extensive evidence that accumulation of mononuclear phagocytes including microglial cells, monocytes, and macrophages at sites of β-amyloid (Aβ) deposition in the brain is an important pathological feature of Alzheimer's disease (AD) and related animal models, and the concentration of these cells clustered around Aβ deposits is several folds higher than in neighboring areas of the brain [1-5]. Microglial cells phagocytose and clear debris, pathogens, and toxins, but they can also be activated to produce inflammatory cytokines, chemokines, and neurotoxins [6]. Over the past decade, the roles of microglial cells in AD have begun to be clarified, and we proposed that these cells play a dichotomous role in the pathogenesis of AD [4, 6-11]. Microglial cells are able to clear soluble and fibrillar Aβ, but continued interactions of these cells with Aβ can lead to an inflammatory response resulting in neurotoxicity. Inflammasomes are inducible high molecular weight protein complexes that are involved in many inflammatory pathological processes. Recently, Aβ was found to activate the NLRP3 inflammasome in microglial cells in vitro and in vivo thereby defining a novel pathway that could lead to progression of AD [12-14]. In this manuscript, we review possible steps leading to Aβ-induced inflammasome activation and discuss how this could contribute to the pathogenesis of 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.