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Microglia receptors and their implications in the response to amyloid β for Alzheimer’s disease pathogenesis
Open accessAbstract
Alzheimer's disease (AD) is a major public health problem with substantial economic and social impacts around the world. The hallmarks of AD pathogenesis include deposition of amyloid β (Aβ), neurofibrillary tangles, and neuroinflammation. For many years, research has been focused on Aβ accumulation in senile plaques, as these aggregations were perceived as the main cause of the neurodegeneration found in AD. However, increasing evidence suggests that inflammation also plays a critical role in the pathogenesis of AD. Microglia cells are the resident macrophages of the brain and act as the first line of defense in the central nervous system. In AD, microglia play a dual role in disease progression, being essential for clearing Aβ deposits and releasing cytotoxic mediators. Aβ activates microglia through a variety of innate immune receptors expressed on these cells. The mechanisms through which amyloid deposits provoke an inflammatory response are not fully understood, but it is believed that these receptors cooperate in the recognition, internalization, and clearance of Aβ and in cell activation. In this review, we discuss the role of several receptors expressed on microglia in Aβ recognition, uptake, and signaling, and their implications for AD pathogenesis.
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“FCγR activation also promotes Aβ clearance via phagocytosis [139, 140].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [140]
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“Microglial LRP1 mediates Aβ uptake and activation of microglia (20–22).”
From LRPAP1 is released from activated microglia and inhibits microglial phagocytosis and amyloid beta aggregation (2023) · cites this paper as [20]
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“Aβ fibrils also increase inflammation148 (Fig. 5, purple), which may unanchor residual PDE4A125, and further disinhibit stress signaling pathways.”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [148]
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“In mouse macrophages and COS cells, SHIP1 was shown to activate the ITIM of the inhibitory receptor FCγRIIβ, which inhibits the activating receptor FCγRIIA to block FCγRIIA-mediated phagocytosis (Fig. 3C).”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [140]
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“SHIP1 also was shown to directly inhibit FCγRIIA by binding to its ITAM (Fig. 3C), which prevents the activation of PI3K [134, 137–140].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [140]
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Cites
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Metadata
- Authors
- Doens, D., & Fernández, P. L.
- Affiliations
- Acharya Nagarjuna University (IN)
- Instituto de Investigaciones Científicas y Servicios de Alta Tecnología (PA)
- Corresponding author
- Fernández, Patricia L
- Venue
- Journal of Neuroinflammation
- Published
- 2014
- Volume
- 11
- Issue
- 1
- Pages
- 48
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3975152
- OpenAlex
- W2100011299
- Cited by
- 348
- References
- 172
- Citations by year
- 2026: 22 · 2025: 42 · 2024: 33 · 2023: 33 · 2022: 36 · 2021: 27 · 2020: 24 · 2019: 24 · 2018: 27 · 2017: 26 · 2016: 24 · 2015: 25 · 2014: 5
- FWCI
- 2.16
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Greater South Information System
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, innate immune receptors, neuroinflammation, amyloid clearance, receptor signaling, microglial activation, amyloid plaques, neurodegeneration
- MeSH terms
- Alzheimer Disease, Animals, Humans, Receptors, Immunologic, Amyloid beta-Peptides, Microglia
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