New Mouse Model of Alzheimer’s
Open accessAbstract
Amyloid β-peptide (Aβ) accumulation is a key characteristic of Alzheimer's disease (AD); therefore, mouse models of AD exhibiting Aβ pathology are valuable tools for unraveling disease mechanisms. However, the overexpression of Aβ precursor protein (APP) used in previous mouse models may cause Aβ-independent artifacts that influence data interpretation. To circumvent these problems, we used an APP knock-in (KI) strategy to introduce mutations to the mouse APP gene to develop a new generation of AD mouse models. These new models, termed APP(NL-F) and APP(NL-G-F), have endogenous APP levels and develop robust Aβ amyloidosis, which induce synaptic degeneration and memory impairments. Thus, we suggest that these novel APP KI mice will serve as important tools to elucidate molecular mechanisms of AD.
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The result in female mice is consistent with the cognitive phenotype in the Y maze reported in this genotype.
“Our result in female mice is consistent with the cognitive phenotype in the Y maze reported in this genotype25,42.”
From Integrated analysis of behavioral, epigenetic, and gut microbiome analyses in AppNL-G-F, AppNL-F, and wild type mice (2021) · cites this paper as [42]
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A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline
Jonsson, T., Atwal, J. K., Steinberg, S., Snaedal, J., Jonsson, P. V., Bjornsson, S., Stefansson, H., Sulem, P., Gudbjartsson, D., Maloney, J., et al. (2012) · Nature · doi:10.1038/nature11283 · Cited by 1,738 · see citing works
Single App knock-in mouse models of Alzheimer’s disease
Saito, T., Matsuba, Y., Mihira, N., Takano, J., Nilsson, P., Itohara, S., Iwata, N., & Saido, T. C. (2014) · Nature Neuroscience · doi:10.1038/nn.3697 · Cited by 1,447 · see citing works
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The Cellular Phase of Alzheimer’s Disease
De Strooper, B., & Karran, E. (2016) · Cell · doi:10.1016/j.cell.2015.12.056 · Cited by 1,990 · see citing works
Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone
Purro, S. A., Farrow, M. A., Linehan, J., Nazari, T., Thomas, D. X., Chen, Z., Mengel, D., Saito, T., Saido, T., Rudge, P., et al. (2018) · Nature · doi:10.1038/s41586-018-0790-y · Cited by 191 · see citing works
Self-citationCastillo, E., Leon, J., Mazzei, G., Abolhassani, N., Haruyama, N., Saito, T., Saido, T., Hokama, M., Iwaki, T., Ohara, T., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-17999-3 · Cited by 158 · see citing works
Self-citationCalpain Activation in Alzheimer's Model Mice Is an Artifact of APP and Presenilin Overexpression
Saito, T., Matsuba, Y., Yamazaki, N., Hashimoto, S., & Saido, T. C. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.1907-16.2016 · Cited by 121 · see citing works
Self-citationKundu, P., Torres, E. R. S., Stagaman, K., Kasschau, K., Okhovat, M., Holden, S., Ward, S., Nevonen, K. A., Davis, B. A., Saito, T., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-83851-4 · Cited by 75 · see citing works
Self-citationInsights on the Use of Transgenic Mice Models in Alzheimer’s Disease Research
Pádua, M. S., Guil-Guerrero, J. L., Prates, J. A. M., & Lopes, P. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25052805 · Cited by 46 · see citing works
Amyloid β induces interneuron-specific changes in the hippocampus of APPNL-F mice
Sos, K. E., Mayer, M. I., Takács, V. T., Major, A., Bardóczi, Z., Beres, B. M., Szeles, T., Saito, T., Saido, T. C., Mody, I., et al. (2020) · PLOS ONE · doi:10.1371/journal.pone.0233700 · Cited by 37 · see citing works
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- Authors
- Nilsson, P., Saito, T., & Saido, T. C.
- Affiliations
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Nilsson, Per
- Saido, Takaomi C
- Venue
- ACS Chemical Neuroscience
- Publisher
- American Chemical Society (ACS)
- Published
- 2014-05-22
- Volume
- 5
- Issue
- 7
- Pages
- 499-502
- ISSN
- 1948-7193 (ISSN-L)
- PMC
- PMC4102956
- OpenAlex
- W2080034260
- Cited by
- 107
- References
- 2
- Citations by year
- 2026: 8 · 2025: 12 · 2024: 17 · 2023: 16 · 2022: 7 · 2021: 10 · 2020: 5 · 2019: 6 · 2018: 10 · 2017: 8 · 2016: 5 · 2015: 3
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- ACS Chemical Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cell Science Research Foundation
- Ministry of Health, Labour and Welfare
- Japan Society for the Promotion of Science (26290019)
- Japan Science and Technology Agency
- RIKEN
- RIKEN Brain Science Institute
- Precursory Research for Embryonic Science and Technology
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, APP knock-in mice, APP mutations, amyloidosis, synaptic degeneration, memory impairment, mouse models of Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Calcium-Binding Proteins, Disease Models, Animal, Humans, Memory Disorders, Mice, Transgenic, Mutation, Amyloid beta-Protein Precursor, Mice, Knockout, Gene Knockout Techniques, Gene Knock-In Techniques
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