Concomitant astroglial atrophy and astrogliosis in a triple transgenic animal model of Alzheimer's disease
Abstract
Astrocytes are fundamental for brain homeostasis and are at the fulcrum of neurological diseases including Alzheimer's disease (AD). Here, we monitored changes in astroglia morphology throughout the age-dependent progression of AD. We used an immunohistochemical approach that allows us to determine the domain of glial cytoskeleton, by measuring the surface, volume, and the relationship between astrocytes and neuritic plaques. We investigated astroglia in the hippocampus of a triple transgenic mouse model of AD (3xTg-AD) that mimics the progression of the human disease. The numerical density of astrocytes is affected neither by AD nor by age. We found reduction of surface and volume of GFAP profiles from early ages (6 months; 43.84 and 52.76%, respectively), persisting at 12 (40.73 and 45.39%) and 18 months (64.80 and 71.95%) in the dentate gyrus (DG) of 3xTg-AD, whereas in CA1 it appears at 18 months (29.42 and 32.74%). This cytoskeleton atrophy is accompanied by a significant reduction of glial somata volume in DG at 12 and 18 months (40.46 and 75.55%, respectively), whereas in CA1 it is significant at 18 months (42.81%). However, while astroglial atrophy appears as a generalized process, astrocytes surrounding plaques are clearly hypertrophic as revealed by increased surface (48.06%; 66.66%), and volume (57.10%; 71.06%) of GFAP profiles in DG and CA1, respectively, at 18 months. We suggest differential effects of AD on astroglial populations depending on their association with plaques accounting for the progressive disruption of neural networks connectivity and neurotransmitters imbalance which underlie mnesic and cognitive impairments observed in AD.
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Especially in cortex and HPF, downregulated genes were also enriched for astrocytes, consistent with previous studies on astrodegeneration in cortex and hippocampus.
“Especially in cortex and HPF, downregulated genes were also enriched for astrocytes, which is consistent with previous studies on astrodegeneration in cortex and hippocampus. 77 , 78”
From Diffusion MRI reveals amyloid plaque–associated cellular signatures through spatial transcriptomic integration (2026) · cites this paper as [77]
ST revealed increased microglial and astrocytic gene expression and decreased oligodendrocyte- and neuron-associated signatures.
“ST revealed increased microglial and astrocytic gene expression and decreased oligodendrocyte‐ and neuron‐associated signatures, consistent with previous immunohistochemical and transcriptomic studies. 6 , 8 , 77 , 78”
From Diffusion MRI reveals amyloid plaque–associated cellular signatures through spatial transcriptomic integration (2026) · cites this paper as [77]
Astrocytes play an important role in Aβ clearance via extracellular protease degradation.
“Despite their susceptibility to Aβ, astrocytes play an important role in its clearance via extracellular protease degradation [13].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [13]
Although astrocytes appear more resistant than neurons to degeneration and death, loss of primary and secondary astrocyte branches has been reported in mouse models of AD and ALS, and in patients with multiple sclerosis.
“In addition, although astrocytes appear to be more resistant than neurons to degeneration and death, loss of primary and secondary astrocyte branches has been reported in mouse models of AD27 and ALS18, and in patients with multiple sclerosis (MS)28.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [27]
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Ugbode, C., Hu, Y., Whalley, B., Peers, C., Rattray, M., & Dallas, M. L. (2017) · Biochemical Journal · doi:10.1042/bcj20160505 · Cited by 25 · see citing works
Han, X., Hu, R., Ping, X., Chen, J., Liu, J., Liu, Z., Jin, X., Gao, X., Lin, M., Zhao, Y., et al. (2026) · Alzheimer's & Dementia · doi:10.1002/alz.71908
- Authors
- Olabarria, M., Noristani, H. N., Verkhratsky, A., & Rodríguez, J. J.
- Affiliations
- University of Manchester (GB)
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2010-02-05
- Volume
- 58
- Issue
- 7
- Pages
- 831-838
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2171502370
- Cited by
- 499
- References
- 54
- Citations by year
- 2026: 21 · 2025: 30 · 2024: 35 · 2023: 47 · 2022: 38 · 2021: 44 · 2020: 38 · 2019: 39 · 2018: 38 · 2017: 34 · 2016: 25 · 2015: 32 · 2014: 20 · 2013: 24 · 2012: 14
- FWCI
- 12.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- ASEP (submittedVersion, public-domain)
- Research Explorer (The University of Manchester) (submittedVersion)
- 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 › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, astrocyte activation, astrocytes, glial fibrillary acidic protein, triple transgenic mouse model, hippocampus, dentate gyrus, CA1, neuritic plaques, astrocyte hypertrophy, age-dependent disease progression
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Atrophy, Cytoskeleton, Disease Models, Animal, Gliosis, Hippocampus, Hypertrophy, Immunohistochemistry, Male, Mice, Transgenic, Time Factors, Cell Death, Disease Progression, Cell Size, Cell Shape, Mice, 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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