Microglia and Astrocytes in Alzheimer’s Disease: Significance and Summary of Recent Advances
Open accessAbstract
Alzheimer's disease, one of the most common forms of dementia, is characterized by a slow progression of cognitive impairment and neuronal loss. Currently, approved treatments for AD are hindered by various side effects and limited efficacy. Despite considerable research, practical treatments for AD have not been developed. Increasing evidence shows that glial cells, especially microglia and astrocytes, are essential in the initiation and progression of AD. During AD progression, activated resident microglia increases the ability of resting astrocytes to transform into reactive astrocytes, promoting neurodegeneration. Extensive clinical and molecular studies show the involvement of microglia and astrocyte-mediated neuroinflammation in AD pathology, indicating that microglia and astrocytes may be potential therapeutic targets for AD. This review will summarize the significant and recent advances of microglia and astrocytes in the pathogenesis of AD in three parts. First, we will review the typical pathological changes of AD and discuss microglia and astrocytes in terms of function and phenotypic changes. Second, we will describe microglia and astrocytes' physiological and pathological role in AD. These roles include the inflammatory response, "eat me" and "don't eat me" signals, Aβ seeding, propagation, clearance, synapse loss, synaptic pruning, remyelination, and demyelination. Last, we will review the pharmacological and non-pharmacological therapies targeting microglia and astrocytes in AD. We conclude that microglia and astrocytes are essential in the initiation and development of AD. Therefore, understanding the new role of microglia and astrocytes in AD progression is critical for future AD studies and clinical trials. Moreover, pharmacological, and non-pharmacological therapies targeting microglia and astrocytes, with specific studies investigating microglia and astrocyte-mediated neuronal damage and repair, may be a promising research direction for future studies regarding AD treatment and prevention.
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Misidentifying disease-associated microglia, reactive astrocytes, or rare cell subpopulations can hinder efforts to characterize disease progression and cellular dysfunction in AD.
“For example, misidentifying disease-associated microglia (DAMs), reactive astrocytes, or rare cell subpopulations can hinder efforts to characterize disease progression and cellular dysfunction in AD[58].”
From Comparative analysis of nuclei isolation methods for brain single-nucleus RNA sequencing (2026) · cites this paper as [58]
The section on Aβ seeding, propagation, and clearance links disease-associated microglia and astrocytes to AD progression, while “Typical pathological changes in AD” describes reactive astrocytes’ functional changes. But the paper does not say that misidentifying these cells or rare subpopulations hinders characterization of progression or cellular dysfunction; searches for cell-type misidentification and rare subpopulations found no such discussion. (LLM, conf=0.79)
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- Authors
- Deng, Q., Wu, C., Parker, E., Liu, T. C.-Y., Duan, R., & Yang, L.
- Affiliations
- South China Normal University (CN)
- Augusta University (US)
- Corresponding author
- Duan, Rui
- Yang, Luodan
- Venue
- Aging and disease
- Publisher
- Aging and Disease
- Published
- 2023
- Volume
- 15
- Issue
- 4
- Pages
- 0
- ISSN
- 2152-5250 (ISSN-L)
- PMC
- PMC11272214
- OpenAlex
- W4387196264
- Cited by
- 102
- References
- 302
- Citations by year
- 2026: 38 · 2025: 43 · 2024: 21
- FWCI
- 2.66
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Aging and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (32100918, 31971096, 31771256)
- China Postdoctoral Science Foundation (2022 T150227, SL2022B04J00013)
- National Key Research and Development Program of China (2017YFB0403801)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglia, astrocytes, neuroinflammation, reactive astrocytes, microglial activation, amyloid-beta, synaptic pruning, synaptic loss, remyelination, demyelination, neurodegeneration, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Humans, Microglia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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