Neuronal loss and microgliosis are restricted to the core of Aβ deposits in mouse models of Alzheimer's disease
Open accessAbstract
Amyloid‐β (Aβ) deposits, pathologic tau, and neurodegeneration are major pathological hallmarks of Alzheimer's disease (AD). The relationship between neuronal loss and Aβ deposits is one of the fundamental questions in the pathogenesis of AD. However, this relationship is controversial. One main reason for the conflicting results may be the confounding effects of pathologic tau, which often coexists with Aβ deposits in the brains of AD patients. To clarify the relationship between neuronal loss and Aβ deposits, mouse models of AD, which develop abundant Aβ deposits in the aged brain without pathologic tau, were used to examine the co‐localization of NeuN‐positive neurons, NF‐H‐positive axons, MBP‐positive myelin sheaths, and Aβ deposits. Neuronal loss, as measured by decreased staining of the neuronal cell body, axon, and myelin sheath, as well as the IBA‐1‐positive microglia, was significantly increased in the core area of cerebral Aβ deposits, but not in adjacent areas. Furthermore, neuronal loss in the core area of cerebral Aβ deposits was correlated with Aβ deposit size. These results clearly indicate that neuronal loss is restricted to the core of Aβ deposits, and this restricted loss probably occurs because the Aβ deposit attracts microglia, which cluster in the core area where Aβ toxicity and neuroinflammation toxicity are restrained. These findings may contribute to our understanding of the relationship between neuronal loss and Aβ deposits in the absence of pathologic tau.
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Previous reports have shown that neuron loss in cortical layer V and subiculum, but not in other brain regions, is consistently associated with intraneuronal Aβ42 accumulation, Aβ plaque burden, spatial memory deficits, and working memory impairment in 5xFAD mice.
“previous reports have shown that neuron loss in the cortical layer V and subiculum, but not in other brain regions, is consistently associated with intraneuronal Aβ42 accumulation, Aβ plaque burden, as well as spatial memory deficits and working memory impairment in 5xFAD mice.”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [90]
The Introduction (page unavailable) reports prior findings of neuron loss in cortical layer V and the subiculum, and separately reports a correlation between neuron loss and intraneuronal Aβ42 in 5xFAD mice. The Discussion (page unavailable) reports this paper’s correlation between neuronal loss and Aβ-deposit size. Neither passage establishes the claimed combined association with spatial-memory deficits or working-memory impairment; the Introduction also says earlier studies had not confirmed the relationship between deposits and neuron loss. (LLM, conf=0.88)
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Araya, P., Niemeyer, B., Schade, K., Dunn, L. N., Waugh, K., Busquet, N., Brindley, C., Brown, C., Winkler, C., Lyford, H. R., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113130 · Cited by 7 · see citing works
“24,40,44,87 88–90 Another study revealed decrease neurogenesis in the subgranular zone of the hippocampus DG in 5xFAD mice, 91 which plays an important role in cognitive dysfunction.”
- Authors
- Zhang, J., Wu, N., Wang, S., Yao, Z., Xiao, F., Lu, J., & Chen, B.
- Affiliations
- Capital Medical University (CN)
- Corresponding author
- Chen, Baian
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2021-05-25
- Volume
- 20
- Issue
- 6
- Pages
- e13380-e13380
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC8208784
- OpenAlex
- W3165775737
- Cited by
- 33
- References
- 16
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 11 · 2023: 6 · 2022: 7 · 2021: 1
- FWCI
- 4.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81971005, 81571230)
- 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-beta deposition, neuronal loss, microglial activation, neuroinflammation, mouse models of Alzheimer's disease, axons, myelin sheath, neurodegeneration
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Humans, Male, Neurons, Amyloid beta-Peptides, Microglia, Mice
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