Differential Relationships of Reactive Astrocytes and Microglia to Fibrillar Amyloid Deposits in Alzheimer Disease
Open accessAbstract
Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive. We postulate that astrocytes and microglia may differentially respond to fibrillar amyloid β. Therefore, we quantified the size distribution of dense-core thioflavin-S (ThioS)-positive plaques in the temporal neocortex of 40 AD patients and the microglial and astrocyte responses in their vicinity (≤50 μm) and performed correlations between both measures. As expected, both astrocytes and microglia were clearly spatially associated with ThioS-positive plaques (p = 0.0001, ≤50 μm vs. >50 μm from their edge), but their relationship to ThioS-positive plaque size differed: larger ThioS-positive plaques were associated with more surrounding activated microglia (p = 0.0026), but this effect was not observed with reactive astrocytes. Microglial response to dense-core plaques seems to be proportional to their size, which we postulate reflects a chemotactic effect of amyloid β. By contrast, plaque-associated astrocytic response does not correlate with plaque size and seems to parallel the behavior of plaque-associated neuritic damage.
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Microglial and astrocytic interactions with Aβ amyloid plaques are associated with amyloid plaque development and neuritic damage.
“Microglial and astrocytic interactions with Aβ amyloid plaques have been associated with amyloid plaque development and neuritic damage [81].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [81]
The Abstract (page not available) reports that both cell types are spatially associated with plaques, but only the microglial response increases with plaque size. The Discussion sections on microglial and astrocytic responses link microglia tentatively to plaque-size stabilization and astrocytes to plaque-associated neuritic damage. The study does not establish an association between both glial interactions and plaque development over time. (LLM, conf=0.82)
Experimental — accuracy not yet measuredReactive astrocytes and activated microglia respond differently to Aβ plaque formation; while microglia respond directly to the presence of plaques, astrocytes are associated with neuritic damage that occurs when synapses are already dysfunctional.
“One study showed that reactive astrocytes and activated microglia respond differently to Aβ plaque formation; while microglia respond directly to the presence of plaques, astrocytes are associated with neuritic damage that occurs when synapses are already dysfunctional [81].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [81]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAstrocytes undergo a dynamic phenotypic change from homeostatic to reactive through an intermediate state in response to their microenvironment conditions, namely the presence of Aβ plaques and NFTs.
“These results are consistent with a dynamic phenotypic change of astrocytes from homeostatic to reactive through an intermediate state in response to their microenvironment conditions, namely the presence of Aβ plaques and NFTs23,54–57”
From Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer’s disease (2024) · cites this paper as [55]
The Introduction describes astrocytic responses around amyloid plaques, and the Discussion (‘Astrocytic Response to Amyloid Plaques’; page unavailable) suggests that reactive astrocytes may respond to plaque-associated neuritic damage. The paper does not describe a homeostatic-to-intermediate-to-reactive progression or establish NFTs as a trigger; it also cautions that its postmortem study cannot establish causality. (LLM, conf=0.86)
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- Authors
- Serrano-Pozo, A., Muzikansky, A., Gómez-Isla, T., Growdon, J. H., Betensky, R. A., Frosch, M. P., & Hyman, B. T.
- Affiliations
- Massachusetts General Hospital (US)
- Harvard University (US)
- Corresponding author
- Hyman, Bradley T.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-06
- Volume
- 72
- Issue
- 6
- Pages
- 462-471
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- PMC
- PMC3661683
- OpenAlex
- W1995111570
- Cited by
- 226
- References
- 70
- Citations by year
- 2026: 14 · 2025: 25 · 2024: 21 · 2023: 22 · 2022: 22 · 2021: 25 · 2020: 14 · 2019: 22 · 2018: 20 · 2017: 10 · 2016: 8 · 2015: 16 · 2014: 5 · 2013: 2
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- public-domain
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Massachusetts General Hospital
- National Institutes of Health (AG08487)
- National Institute on Aging (AG008487, R01AG008487, P50AG005134, P30AG062421)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, amyloid plaques, reactive astrocytes, microglial activation, fibrillar amyloid-beta, plaque size, thioflavin S, temporal neocortex, chemotaxis
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Astrocytes, Brain, Female, Humans, Male, Microglia, Plaque, Amyloid
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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