Cited by 213Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Mouse Models of Alzheimer’s Disease

Open access
Yokoyama, Miyabishara, Kobayashi, Honoka, Tatsumi, Lisa, Tomita, Taisuke·2022·Frontiers in Molecular Neuroscience

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fnmol.2022.912995

Cites

128 of 128 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Yokoyama, M., Kobayashi, H., Tatsumi, L., & Tomita, T.
Affiliations
The University of Tokyo (JP)
Corresponding author
Tomita, Taisuke
Venue
Frontiers in Molecular Neuroscience
Published
2022-06-21
Volume
15
Pages
912995-912995
ISSN
1662-5099 (ISSN-L)
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
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

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 ›

Are you an author, or do you see a problem with this page? Request a review