The DOI matches its Crossref record; 119 of the 122 references it cites were found in a registry or an index.
Mechanisms of Aβ Clearance and Degradation by Glial Cells
Open accessAbstract
Glial cells have a variety of functions in the brain, ranging from immune defense against external and endogenous hazardous stimuli, regulation of synaptic formation, calcium homeostasis, and metabolic support for neurons. Their dysregulation can contribute to the development of neurodegenerative disorders, including Alzheimer's disease (AD). One of the most important functions of glial cells in AD is the regulation of Amyloid-β (Aβ) levels in the brain. Microglia and astrocytes have been reported to play a central role as moderators of Aβ clearance and degradation. The mechanisms of Aβ degradation by glial cells include the production of proteases, including neprilysin, the insulin degrading enzyme, and the endothelin-converting enzymes, able to hydrolyse Aβ at different cleavage sites. Besides these enzymes, other proteases have been described to have some role in Aβ elimination, such as plasminogen activators, angiotensin-converting enzyme, and matrix metalloproteinases. Other relevant mediators that are released by glial cells are extracellular chaperones, involved in the clearance of Aβ alone or in association with receptors/transporters that facilitate their exit to the blood circulation. These include apolipoproteins, α2macroglobulin, and α1-antichymotrypsin. Finally, astrocytes and microglia have an essential role in phagocytosing Aβ, in many cases via a number of receptors that are expressed on their surface. In this review, we examine all of these mechanisms, providing an update on the latest research in this field.
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“Microglia activation reduces the accumulation of Aβ in the brain by increasing its phagocytosis, clearance, and degradation75.”
From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [75]
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.
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“The secretion of Aβ may thus be a normal immune response to any microbe that may invade the nervous system, and if infection clears, the deposited Aβ can be cleared by phagocytic glia71.”
From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [71]
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In the citing paper
“Astrocytes can produce Aβ peptidases, such as neprilysin and IDE as well as the Apolipoprotein E (ApoE) [15]”
From Pharmacological ablation of astrocytes reduces Aβ degradation and synaptic connectivity in an ex vivo model of Alzheimer’s disease (2021) · cites this paper as [15]
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“Neprilysin is mainly expressed in neurons [32] but can also be found in activated astrocytes and microglia [15]”
From Pharmacological ablation of astrocytes reduces Aβ degradation and synaptic connectivity in an ex vivo model of Alzheimer’s disease (2021) · cites this paper as [15]
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“ApoE is mainly produced in astrocytes but can be synthesized by microglia [15].”
From Pharmacological ablation of astrocytes reduces Aβ degradation and synaptic connectivity in an ex vivo model of Alzheimer’s disease (2021) · cites this paper as [15]
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“Indeed, microglia and astrocytes have been shown to play a key role in Aβ clearance and degradation [92].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [92]
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Citations
Cites
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“…Microglia, specialized phagocytic cells of the brain, play a critical role in the clearance of A β , which is involved in the pathogenesis of AD (Ries and Sastre, 2016; Taraso-Conway et al., 2015), The ability of microglia to remove A β is influenced by their cellular cholesterol clearance…”
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Metadata
- Authors
- Ries, M., & Sastre, M.
- Affiliations
- Hammersmith Hospital (GB)
- Corresponding author
- Sastre, Magdalena
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2016-07-05
- Volume
- 8
- Pages
- 160-160
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC4932097
- OpenAlex
- W2460612985
- Cited by
- 527
- References
- 122
- Citations by year
- 2026: 32 · 2025: 53 · 2024: 62 · 2023: 60 · 2022: 77 · 2021: 76 · 2020: 57 · 2019: 47 · 2018: 32 · 2017: 31
- FWCI
- 4.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Spiral (Imperial College London) (submittedVersion, other-oa)
- Funders
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Cerebrospinal fluid and hydrocephalus
- Keywords
- amyloid-beta clearance, amyloid beta degradation, glial cells, microglia, astrocytes, Alzheimer's disease, neprilysin, insulin-degrading enzyme, endothelin-converting enzyme, matrix metalloproteinases, plasminogen activator, angiotensin-converting enzyme, extracellular chaperones, apolipoproteins, alpha2-macroglobulin, alpha-1-antichymotrypsin, phagocytosis
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