Mouse Models of Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and personality changes, eventually leading to dementia. The pathological hallmarks of AD are senile plaques and neurofibrillary tangles, which comprise abnormally aggregated β-amyloid peptide (Aβ) and hyperphosphorylated tau protein. To develop preventive, diagnostic, and therapeutic strategies for AD, it is essential to establish animal models that recapitulate the pathophysiological process of AD. In this review, we will summarize the advantages and limitations of various mouse models of AD, including transgenic, knock-in, and injection models based on Aβ and tau. We will also discuss other mouse models based on neuroinflammation because recent genetic studies have suggested that microglia are crucial in the pathogenesis of AD. Although each mouse model has its advantages and disadvantages, further research on AD pathobiology will lead to the establishment of more accurate mouse models, and accelerate the development of innovative therapeutics.
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Modeling these pathological hallmarks has largely relied on transgenic cellular and animal models harboring genetic mutations linked to ADAD.
“Modeling these pathological hallmarks has largely relied on transgenic cellular and animal models harboring genetic mutations linked to ADAD (3–5).”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [4]
The section “Aβ Deposited Mouse Models Based on APP Mutations” says widely used mouse models carry familial AD-linked APP mutations. The paper does not establish the claim about cellular models, and its “Tauopathy Mouse Models” section says tau models use mutations linked to frontotemporal dementia, not familial AD. No page numbers are available in our copy. (LLM, conf=0.86)
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- Authors
- Yokoyama, M., Kobayashi, H., Tatsumi, L., & Tomita, T.
- Affiliations
- The University of Tokyo (JP)
- Corresponding author
- Tomita, Taisuke
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2022-06-21
- Volume
- 15
- Pages
- 912995-912995
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC9254908
- OpenAlex
- W4283267746
- Cited by
- 213
- References
- 128
- Citations by year
- 2026: 40 · 2025: 63 · 2024: 77 · 2023: 31 · 2022: 1 · 2013: 1
- FWCI
- 5.91
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Japan Society for the Promotion of Science
- Japan Agency for Medical Research and Development
- Moonshot Research and Development Program
- 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, mouse model, transgenic mice, knock-in mice, amyloid-beta, tau protein, neurofibrillary tangles, amyloid plaques, neuroinflammation, microglia
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