β-amyloid, microglia, and the inflammasome in Alzheimer’s disease
Open accessAbstract
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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Microglia-Aβ interactions lead to early synapse loss, production of ROS and RNS, NLRP3 inflammasome activation, and proinflammatory cytokines and TNF.
“Microglia–Aβ interactions lead to early synapse loss39, production of neurotoxic reactive oxygen and nitrogen species (ROS and RNS), NLRP3 inflammasome activation, and production of proinflammatory cytokines and TNF27,40–42.”
From Microglia in neurodegeneration (2018) · cites this paper as [41]
Increasing evidence supports the hypothesis that the microglial response to AD lesions controls disease progression.
“Increasing evidence supports the hypothesis that the microglial response to AD lesions controls disease progression”
From TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease (2017) · cites this paper as Gold and El Khoury, 2015
NLRP3 inflammasome assembly and activation regulates activation of caspase-1, which catalyzes cleavage and activation of proinflammatory cytokines of the IL-1β family, promoting secretion of biologically active cytokines; these cytokines could induce neuronal degeneration.
“Their assembly and activation regulates activation of caspase-1, which catalyzes the cleavage and activation of proinflammatory cytokines of the IL-1β family, promoting the secretion of these, now biologically active, cytokines. These cytokines could induce neuronal degeneration (Gold and El Khoury, 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Gold and El Khoury, 2015
NLRP3 inflammasome activation reduces phagocytosis of Aβ by microglial cells, thus increasing Aβ depositions and contributing to the pathogenesis of AD.
“In addition, NLRP3 inflammasome activation reduces phagocytosis of Aβ by microglial cells, thus increasing the Aβ depositions and contributing to the pathogenesis of AD (Garlanda et al., 2013; Gold and El Khoury, 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Gold and El Khoury, 2015
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- Authors
- Gold, M., & El Khoury, J.
- Affiliations
- Harvard University (US)
- Venue
- Seminars in Immunopathology
- Published
- 2015-08-07
- Volume
- 37
- Issue
- 6
- Pages
- 607-611
- ISSN
- 1863-2297 (ISSN-L)
- 1863-2300
- PMC
- PMC4618770
- OpenAlex
- W1883181368
- Cited by
- 187
- References
- 62
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 15 · 2023: 17 · 2022: 17 · 2021: 22 · 2020: 22 · 2019: 25 · 2018: 22 · 2017: 23 · 2016: 11
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Seminars in Immunopathology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Max Kade Foundation
- National Institutes of Health
- National Institute on Aging (RF1AG051506, AG032349, R01AG032349)
- National Institute of Allergy and Infectious Diseases (AI082660, U24AI082660)
- National Institute of Neurological Disorders and Stroke (NS059005, R01NS059005)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- Alzheimer's disease, amyloid-beta, microglia, inflammasome, NLRP3 inflammasome, neuroinflammation, monocytes, macrophages, neurotoxicity, amyloid clearance, pathogenesis
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Alzheimer Disease, Brain, Carrier Proteins, Humans, Macrophages, Monocytes, Phagocytosis, Cytokines, Amyloid beta-Peptides, Microglia, Inflammasomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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