The DOI matches its Crossref record; 172 of the 173 references it cites were found in a registry or an index, and 1 are not checked yet.
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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1 retracted
Retracted: ‘Clinical trials in Alzheimer’s disease’: immunotherapy approaches
Delrieu, J., Ousset, P., Caillaud, C., & Vellas, B. J. (2011) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2011.07458.x · Cited by 147
RetractedThe Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
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Gout-associated uric acid crystals activate the NALP3 inflammasome
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Cytokine-mediated regulation of CXCR4 expression in human neutrophils
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TREM2 Variants in Alzheimer's Disease
Guerreiro, R., Wojtas, A., Bras, J., Carrasquillo, M., Rogaeva, E., Majounie, E., Cruchaga, C., Sassi, C., Kauwe, J. S. K., Younkin, S., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1211851 · Cited by 3,020
NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
Heneka, M. T., Kummer, M. P., Stutz, A., Delekate, A., Schwartz, S., Vieira-Saecker, A., Griep, A., Axt, D., Remus, A., Tzeng, T.-C., et al. (2013) · Nature · doi:10.1038/nature11729 · Cited by 2,898
Research works printed but not linked: 1
- 10.1146/annurev.bi.63.070194.003125 · DOI
Cited by
Sorted by citations
Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
Leng, F., & Edison, P. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-020-00435-y · Cited by 3,179
The Gut Microbiota and Alzheimer’s Disease
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TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function
Zhao, Y., Wu, X., Li, X., Jiang, L.-L., Gui, X., Liu, Y., Sun, Y., Zhu, B., Piña-Crespo, J. C., Zhang, M., et al. (2018) · Neuron · doi:10.1016/j.neuron.2018.01.031 · Cited by 763
Stress weakens prefrontal networks: molecular insults to higher cognition
Arnsten, A. F. T. (2015) · Nature Neuroscience · doi:10.1038/nn.4087 · Cited by 752
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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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