Microglia prevent beta-amyloid plaque formation in the early stage of an Alzheimer’s disease mouse model with suppression of glymphatic clearance
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Abstract
Background: Soluble beta-amyloid (Aβ) can be cleared from the brain through various mechanisms including enzymatic degradation, glial cell phagocytosis, transport across the blood-brain barrier, and glymphatic clearance. However, the relative contribution of each clearance system and their compensatory effects in delaying the pathological process of Alzheimer’s disease (AD) are currently unknown. Methods: Fluorescent trace, immunofluorescence, and Western blot analyses were performed to compare glymphatic clearance ability and Aβ accumulation among 3-month-old APP695/PS1-dE9 transgenic (APP/PS1) mice, wild-type mice, aquaporin 4 knock out (AQP4 −/− ) mice, and AQP4 −/− /APP/PS1 mice. The consequence of selectively eliminating microglial cells, or downregulating apolipoprotein E (apoE) expression, on Aβ burden, was also investigated in the frontal cortex of AQP4 −/− /APP/PS1 mice and APP/PS1 mice. Results: AQP4 deletion in APP/PS1 mice significantly exaggerated glymphatic clearance dysfunction, and intraneuronal accumulation of Aβ and apoE, although it did not lead to Aβ plaque deposition. Notably, microglia, but not astrocytes, increased activation and phagocytosis of Aβ in the cerebral cortex of AQP4 −/− /APP/PS1 mice, compared with APP/PS1 mice. Selectively eliminating microglia in the frontal cortex via local injection of clodronate liposomes resulted in deposition of Aβ plaques in AQP4 −/− /APP/PS1 mice, but not APP/PS1 mice. Moreover, knockdown of apoE reduced intraneuronal Aβ levels in both APP/PS1 mice and AQP4 −/− /APP/PS1 mice, indicating an inhibitory effect of apoE on Aβ clearance. Conclusion: The above results suggest that the glymphatic system mediated Aβ and apoE clearance and microglia mediated Aβ degradation synergistically prevent Aβ plague formation in the early stages of the AD mouse model. Protecting one or both of them might be beneficial to delaying the onset of AD.
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In the early stages of AD, activated microglia cause phagocytosis and clearance of pathologic Aβ and/or tau, positively affecting AD pathologies in animal models.
“In the early stages of AD, activated microglia cause phagocytosis and clearance of pathologic Aβ and/or tau, positively affecting AD pathologies in animal models [89, 90].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [90]
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- Authors
- Feng, W., Zhang, Y., Wang, Z., Xu, H., Wu, T., Marshall, C., Gao, J., & Xiao, M.
- Affiliations
- Nanjing Brain Hospital (CN)
- Jiangsu Province Hospital (CN)
- University of Kentucky (US)
- Corresponding author
- Gao, Junying
- Xiao, Ming
- Venue
- Alzheimer's Research & Therapy
- Published
- 2020-10-02
- Volume
- 12
- Issue
- 1
- Pages
- 125-125
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC7532614
- OpenAlex
- W3090445757
- Cited by
- 150
- References
- 65
- Citations by year
- 2026: 20 · 2025: 27 · 2024: 27 · 2023: 35 · 2022: 25 · 2021: 15 · 2020: 1
- FWCI
- 11.39
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion, cc-by)
- Research Square (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81671070, 81772454)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- Alzheimer's disease, amyloid-beta, glymphatic system, microglia, aquaporin-4, apolipoprotein E, amyloid plaque formation, APP/PS1 mice, clodronate liposomes, microglial phagocytosis, amyloid clearance, astrocytes
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Mice, Transgenic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Mice, Presenilin-1, Plaque, Amyloid
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