Accelerated microglial pathology is associated with A β plaques in mouse models of A lzheimer's disease
Open accessAbstract
Microglia integrate within the neural tissue with a distinct ramified morphology through which they scan the surrounding neuronal network. Here, we used a digital tool for the quantitative morphometric characterization of fine cortical microglial structures in mice, and the changes they undergo with aging and in Alzheimer's-like disease. We show that, compared with microglia in young mice, microglia in old mice are less ramified and possess fewer branches and fine processes along with a slightly increased proinflammatory cytokine expression. A similar microglial pathology appeared 6-12 months earlier in mouse models of Alzheimer's disease (AD), along with a significant increase in brain parenchyma lacking coverage by microglial processes. We further demonstrate that microglia near amyloid plaques acquire unique activated phenotypes with impaired process complexity. We thus show that along with a chronic proinflammatory reaction in the brain, aging causes a significant reduction in the capacity of microglia to scan their environment. This type of pathology is markedly accelerated in mouse models of AD, resulting in a severe microglial process deficiency, and possibly contributing to enhanced cognitive decline.
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Plaque-associated microglia exhibit morphological and molecular differences compared to non-plaque-associated cells in AD.
“Plaque-associated microglia exhibit morphological and molecular differences compared to non-plaque-associated cells in AD44,45,46.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [45]
The Results section, “Differential pattern of CD39 expression in plaque-associated microglia” (page unavailable), describes differences in morphology and CD39 and activation-marker expression among microglia near plaques and in the surrounding tissue. The study examines mouse models of AD, however, so it does not establish the comparison in human AD. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThis impairment has been shown to correlate with increased production of proinflammatory cytokines and overwhelming accumulation of Aβ plaques in the AD brain.
“This impairment has been shown to correlate with increased production of proinflammatory cytokines and overwhelming accumulation of Aβ plaques in the AD brain [20–22].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [21]
The Results section on APP transgenic mice and the Discussion associate impaired microglial coverage with Aβ plaques in mouse models. The reported cytokine increase was measured during aging in wild-type mice; the Discussion cautions that plaque-associated microglial changes do not readily translate into robust cytokine upregulation. The paper therefore does not establish the full correlation claimed for the human AD brain. (LLM, conf=0.86)
Experimental — accuracy not yet measuredP2ry12 is expressed in highly ramified iMGLs resembling quiescent cortical microglia.
“At higher magnification, P2ry12 is expressed in highly ramified iMGLs resembling quiescent cortical microglia; the membrane distribution accentuates the finer extended processes (Figure 7B–D)(Baron et al., 2014).”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Baron et al., 2014
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- Authors
- Baron, R., Babcock, A. A., Nemirovsky, A., Finsen, B., & Monsonego, A.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- University of Southern Denmark (DK)
- Corresponding author
- Monsonego, Alon
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2014-03-18
- Volume
- 13
- Issue
- 4
- Pages
- 584-595
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC4326940
- OpenAlex
- W2068354213
- Cited by
- 118
- References
- 49
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 5 · 2023: 7 · 2022: 8 · 2021: 19 · 2020: 6 · 2019: 11 · 2018: 8 · 2017: 12 · 2016: 14 · 2015: 14 · 2014: 3
- FWCI
- 7.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Israel Science Foundation
- Danish Medical Research Council
- Lundbeck Foundation
- The Danish Alzheimer Research Foundation
- 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
- microglia, Alzheimer's disease, amyloid plaques, microglial ramification, microglial morphology, aging, inflammatory cytokines, microglial activation, cognitive decline, mouse models of Alzheimer's disease, cortical microglia
- MeSH terms
- Aging, Alzheimer Disease, Animals, Apyrase, Cerebral Cortex, Disease Models, Animal, Mice, Transgenic, Antigens, CD, Cytokines, Amyloid beta-Peptides, Leukocyte Common Antigens, Microglia, Inflammation Mediators, CD11b Antigen, Cell Shape, Green Fluorescent Proteins, Mice, Plaque, Amyloid
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