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Autophagy in microglia degrades extracellular β-amyloid fibrils and regulates the NLRP3 inflammasome
Open accessAbstract
Accumulation of β-amyloid (Aβ) and resultant inflammation are critical pathological features of Alzheimer disease (AD). Microglia, a primary immune cell in brain, ingests and degrades extracellular Aβ fibrils via the lysosomal system. Autophagy is a catabolic process that degrades native cellular components, however, the role of autophagy in Aβ degradation by microglia and its effects on AD are unknown. Here we demonstrate a novel role for autophagy in the clearance of extracellular Aβ fibrils by microglia and in the regulation of the Aβ-induced NLRP3 (NLR family, pyrin domain containing 3) inflammasome using microglia specific atg7 knockout mice and cell cultures. We found in microglial cultures that Aβ interacts with MAP1LC3B-II via OPTN/optineurin and is degraded by an autophagic process mediated by the PRKAA1 pathway. We anticipate that enhancing microglial autophagy may be a promising new therapeutic strategy for AD.
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“However, enhancing A β uptake/efflux without simultaneously improving intracellular degradative capacity may impose an additional proteostatic burden on cells [ 28, 31 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [28]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In AD, autophagic flux is impaired, exacerbating A β deposition [ 28, 29 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [28]
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“one study showed that microglial autophagy facilitates clearance of extracellular Aβ fibrils and reduces Aβ-induced NLRP3 activation (200).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [200]
In the citing paper
“microglial phagocytosis of Aβ deposits in Alzheimer disease models [430,431] requires the autophagy-related factors BECN1, ATG7 and LC3 [432,433].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [432]
In the citing paper
“autophagy may also enhance microglial clearance of Aβ”
From TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease (2017) · cites this paper as Cho et al., 2014
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Metadata
- Authors
- Cho, M.-H., Cho, K., Kang, H.-J., Jeon, E.-Y., Kim, H.-S., Kwon, H.-J., Kim, H.-M., Kim, D.-H., & Yoon, S.-Y.
- Affiliations
- Asan Medical Center (KR)
- University of Ulsan (KR)
- Corresponding author
- Yoon, Seung-Yong
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2014-07-22
- Volume
- 10
- Issue
- 10
- Pages
- 1761-1775
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC4198361
- OpenAlex
- W2099588975
- Cited by
- 395
- References
- 47
- Citations by year
- 2026: 26 · 2025: 28 · 2024: 38 · 2023: 45 · 2022: 51 · 2021: 41 · 2020: 49 · 2019: 34 · 2018: 19 · 2017: 30 · 2016: 20 · 2015: 13 · 2014: 1
- FWCI
- 16.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation
- National Research Foundation of Korea (2008-0062286)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- microglia, amyloid-beta, Alzheimer's disease, NLRP3 inflammasome, lysosomal degradation, LC3B, PRKAA1, neuroinflammation
- MeSH terms
- Autophagy-Related Protein 7, NLR Family, Pyrin Domain-Containing 3 Protein, Sequestosome-1 Protein, Aged, Aged, 80 and over, Alzheimer Disease, Animals, Autophagy, Carrier Proteins, Cell Line, Extracellular Space, Eye Proteins, Female, Heat-Shock Proteins, Humans, Inflammation, Male, Microtubule-Associated Proteins, Models, Biological, Neurons, Amyloid beta-Peptides, Microglia, Cell Cycle Proteins, Integrases, Membrane Transport Proteins, Transcription Factor TFIIIA, Adaptor Proteins, Signal Transducing, Mice, AMP-Activated Protein Kinases, Inflammasomes, Proteolysis
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