Single App knock-in mouse models of Alzheimer’s disease
Abstract
Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP). These mice, however, suffer from artificial phenotypes because, in addition to amyloid β peptide (Aβ), they overproduce other APP fragments. We generated knock-in mice that harbor Swedish and Beyreuther/Iberian mutations with and without the Arctic mutation in the APP gene. The mice showed typical Aβ pathology, neuroinflammation and memory impairment in an age-dependent manner.
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AppNL-G-F knock-in mice express App under its endogenous promoter in a physiological manner with regards to both cell type and amount, and avoid the issue of APP overexpression and abnormal expression patterns.
“We elected to use the AppNL-G-F knock-in mouse model for this study as it expresses App under its endogenous promoter in a physiological manner with regards to both cell type and amount, and avoids the issue of APP overexpression and abnormal expression patterns.”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [33]
AppNL-G-F mice were provided by the RIKEN BRC through the National BioResource Project of the MEXT, Japan.
“AppNL-G-F mice [C57BL/6-App<tm3(NL-G-F)Tcs> (No.RBRC06344)] were provided by the RIKEN BRC through the National BioResource Project of the MEXT, Japan [33].”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [33]
APPNLGF knock-in mice express a humanized and triple-mutated APP in the endogenous App locus, which circumvents transgenic mouse artifacts.
“we employed APPNLGF knock-in mice that express a humanized and triple-mutated APP in the endogenous App locus to circumvent transgenic mouse artifacts.”
From Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice (2024) · cites this paper as [34]
Novel APP knock-in models such as APPNL, APPNL-F, or APPNL-G-F overproduce Aβ1-42 in the absence of potentially confounding APP overexpression, but still contain one or more independent FAD mutations, which might result in an abnormal Aβ conformation.
“While novel APP knock-in models, such as APPNL, APPNL-F, or APPNL-G-F mice overproduce Aβ1–42 in the absence of potentially confounding APP overexpression [139], these mice still contain one or more independent FAD mutations, which might result in an abnormal Aβ conformation [140].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [139]
App NL-G-F mice exhibit a substantial amyloid plaque burden in the brain by 6 months of age.
“By 6 months of age, App NL‐G‐F mice exhibit a substantial amyloid plaque burden in the brain”
From Alzheimer's Protection by <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Saito et al. 2014
The App NL-G-F mouse model is an AD-like model.
“These were bred to the App NL‐G‐F AD‐like model to determine responses in the context of amyloid‐driven pathology (Saito et al. 2014).”
From Alzheimer's Protection by <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Saito et al. 2014
App NL-G-F mice are characterized by progressive amyloid deposition from 2 months to cognitive decline by 6 months.
“The App NL‐G‐F mice are characterized by progressive amyloid deposition from 2 months to cognitive decline by 6 months (Saito et al. 2014).”
From Alzheimer's Protection by <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Saito et al. 2014
The App NL-G-F knock-in model has physiological App expression levels, avoiding the overexpression artifacts found in other transgenic models.
“The App NL‐G‐F knock‐in model, however, has physiological App expression levels, avoiding the overexpression artifacts found in other transgenic models”
From Alzheimer's Protection by <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Saito et al. 2014
The App NL-G-F knock-in model is strongly biased toward very high Aβ42:40 ratios (~10-100:1) because of the familial mutations.
“but is strongly biased toward very high Aβ42:40 ratios (~10–100:1) because of the familial mutations”
From Alzheimer's Protection by <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Saito et al. 2014
In AppNL-G-F mice, Aβ amyloidosis is aggressive, and neuroinflammation is observed in subcortical structures as well as cortical regions.
“In AppNL-G-F mice, which harbor all three mutations, Aβ amyloidosis is aggressive, and neuroinflammation is observed in subcortical structures as well as cortical regions [10–12].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
AppNL mice produce significantly higher levels of Aβ40 and Aβ42 without overt AD-related brain pathology such as extracellular Aβ plaques or neuroinflammation.
“By contrast, AppNL mice that carry only the Swedish mutation produce significantly higher levels of Aβ40 and Aβ42 without overt AD-related brain pathology such as extracellular Aβ plaques or neuroinflammation [10, 11, 13].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
AppNL-G-F mice harbor three familial AD mutations (Swedish, Beyreuther/Iberian, and Arctic).
“alternative mouse models have been generated via knock-in (KI) of a humanized Aβ sequences harboring familial AD mutations (Swedish (NL), Beyreuther/Iberian (F), and Arctic (G)) in order to model Aβ amyloidosis without non-physiological overexpression of APP [10].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
AppNL mice harbor only the Swedish mutation.
“By contrast, AppNL mice that carry only the Swedish mutation produce significantly higher levels of Aβ40 and Aβ42 without overt AD-related brain pathology such as extracellular Aβ plaques or neuroinflammation [10, 11, 13].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
KI mouse models with familial AD mutations have been generated to overcome these issues.
“To overcome these issues, KI mouse models with familial AD mutations have been generated [10, 24, 31, 32].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
AppNL/NL mice overproduce human Aβ40 and Aβ42 in their brains.
“despite overproducing human Aβ40 and Aβ42 in their brains [10, 13].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
Recent studies reported negligible cognitive deficits and lack of Aβ plaque formation in AppNL/NL mice.
“These results are consistent with recent studies reporting negligible cognitive deficits and the lack of Aβ plaque formation in AppNL/NL mice (Fig. 6) [10, 11, 13, 14, 24].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [10]
Both AppNL-F and AppNL-G-F models express human APP at physiological levels.
“Both models express human APP at physiological levels.”
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 [25]
The AppNL-G-F and AppNL-F show neuropathology and hippocampus-dependent cognitive impairments at 6 or 18 months, respectively.
“The AppNL-G-F and AppNL-F show neuropathology and hippocampus-dependent cognitive impairments at 6 or 18 months, respectively.”
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 [25]
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 [25]
Human APP knockin (KI) models develop robust Aβ pathology, yet do not exhibit artifacts associated with APP over-expression, such as elevated levels of APP cleavage products.
“Human APP knockin (KI) models develop robust Aβ pathology, yet do not exhibit artifacts associated with APP over-expression, such as elevated levels of APP cleavage products (Saito et al., 2014).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
These studies all suffer because they exhibit artifacts arising from the over-expression APP (WT or mutant) and in some cases mutant presenilins.
“These studies all suffer because they exhibit artifacts arising from the over-expression APP (WT or mutant) and in some cases mutant presenilins (Balducci and Forloni, 2011; Saito et al., 2014; Sasaguri et al., 2017).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
Human MAPT knock-in models produce tau pathology, but only very late in the murine life span (~15 months).
“Human MAPT knock-in models have also been developed, and these models produce tau pathology, but only very late in the murine life span (~15 months) (Saito et al., 2014; Sakakibara et al., 2018; Sasaguri et al., 2022).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
Over-expressing APP and presenilin 1 cause effects resulting from the over-expression that are unrelated to the disease process.
“However, over-expressing APP and presenilin 1 cause effect resulting from the over-expression that are unrelated to the disease process (Saito et al., 2014; Sakakibara et al., 2018).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
Knock-in human APP mice develop robust plaque pathology beginning as early as 3 months of age, however they develop little tau pathology and little neurodegeneration.
“These mice develop robust plaque pathology beginning as early as 3 months of age, however they develop little tau pathology and little neurodegeneration (Saito et al., 2014; Sakakibara et al., 2018).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
The patterns of labeling of Aβ and MAPT are consistent with prior studies of APPNL-G-F and P301S MAPT mice.
“These patterns of labeling or Aβ and MAPT are consistent with prior studies of APPNL-G-F and P301S MAPT mice (Yoshiyama et al., 2007; Saito et al., 2014; Sasaguri et al., 2017; Apicco et al., 2018).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Saito et al., 2014
22-month-old AppNL-G-F mice had robust AD-related pathology, including amyloid deposition and neuroinflammation.
“As expected,15 22-month-old AppNL-G-F mice had robust AD-related pathology, including amyloid deposition and neuroinflammation (Figures 1C and 1D).”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [15]
App KI mice may model preclinical stages of AD, characterized by progressive amyloidosis and gliosis without prominent cognitive deterioration, tau pathology, or neurodegeneration.
“As suggested,15,20 App KI mice may model pre-clinical stages of AD, characterized by progressive amyloidosis and gliosis without prominent cognitive deterioration, tau pathology, or neurodegeneration.”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [15]
Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.
“Humanized App knockin (KI) and APP transgenic mouse models mimic certain aspects of AD pathogenesis, including progressive amyloidosis, gliosis, and neuroinflammation, as well as network hyperexcitability and cognitive impairment, albeit to different degrees of severity across models and paradigms.15-27”
From Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models (2024) · cites this paper as [15]
We show in a well-studied App knock-in mouse model the gradual establishment of a multicellular co-expressed gene response encompassing 57 Plaque-Induced Genes or PIGs in the microenvironments of amyloid plaques.
“We show in a well-studied App knock-in mouse model (Saito et al. , 2014) the gradual establishment of a multicellular co-expressed gene response encompassing 57 Plaque-Induced Genes or PIGs in the microenvironments of amyloid plaques (Figure 5).”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Saito et al., 2014
App NL-G-F knock-in mice express Swedish (KM670/671NL), Beyreuther/Iberian (I716F), and Arctic (E693G) mutations in the App gene under the endogenous promoter on the C57Bl/6J background.
“App NL-G-F knock-in (Saito et al., 2014) mice express Swedish (KM670/671NL), Beyreuther/Iberian (I716F), and Arctic (E693G) mutations in the App gene under the endogenous promoter on the C57Bl/6J background.”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Saito et al., 2014
AD mice have APP with a humanised Aβ region containing 3 AD-related mutations (APPNL-G-F) knocked in, to avoid artefacts associated with over-expressing APP.
“AD mice, in which APP with a humanised Aβ region containing 3 AD-related mutations (APPNL-G-F) is knocked in (49), to avoid artefacts associated with over-expressing APP, were crossed with NG2-DsRed mice in which pericytes express DsRed (19).”
From Amyloid β oligomers constrict human capillaries in Alzheimer's disease via signaling to pericytes (2019) · cites this paper as [49]
Knock-in of Swedish and Iberian mutations results in plaque development beginning at 6 months, and gliosis, synaptic alterations and memory impairment from 18 months.
“In contrast, knock-in of Swedish and Iberian mutations results in plaque development beginning at 6 months, and gliosis, synaptic alterations and memory impairment from 18 months [129].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [129]
Additional knock-in of the Arctic mutation into these mice results in more rapid pathology development including plaque development beginning at 2 months that is more widespread throughout the brain and memory impairment from 6 months.
“Additional knock-in of the Arctic mutation into these mice results in more rapid pathology development including plaque development beginning at 2 months that is more widespread throughout the brain and memory impairment from 6 months [129].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [129]
Initial studies show that more physiological knock-in mouse models develop cognitive impairment many months after plaque development, which is more similar to humans.
“In contrast, initial studies show that more physiological knock-in mouse models develop cognitive impairment many months after plaque development [129], which is more similar to humans.”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [129]
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Self-citationDionísio, P. A., Amaral, J. D., Ribeiro, M. F., Lo, A. C., D'Hooge, R., & Rodrigues, C. M. P. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.08.034 · Cited by 127 · see citing works
Fairley, L. H., Lai, K. O., Wong, J. H., Chong, W. J., Vincent, A. S., D’Agostino, G. A., Wu, X., Naik, R. R., Jayaraman, A., Langley, S. R., et al. (2023) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2209177120 · Cited by 127 · see citing works
Neuroinflammation in Alzheimer’s disease: microglial signature and their relevance to disease
Sobue, A., Komine, O., & Yamanaka, K. (2023) · Inflammation and Regeneration · doi:10.1186/s41232-023-00277-3 · Cited by 127 · see citing works
Petrache, A. L., Rajulawalla, A., Shi, A., Wetzel, A., Saito, T., Saido, T. C., Harvey, K., & Ali, A. B. (2019) · Cerebral Cortex · doi:10.1093/cercor/bhz016 · Cited by 124 · see citing works
Self-citation
- Authors
- Saito, T., Matsuba, Y., Mihira, N., Takano, J., Nilsson, P., Itohara, S., Iwata, N., & Saido, T. C.
- Affiliations
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Saido, Takaomi C
- Venue
- Nature Neuroscience
- Published
- 2014-04-13
- Volume
- 17
- Issue
- 5
- Pages
- 661-663
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2090620788
- Cited by
- 1,447
- References
- 26
- Citations by year
- 2026: 128 · 2025: 167 · 2024: 213 · 2023: 164 · 2022: 168 · 2021: 156 · 2020: 97 · 2019: 71 · 2018: 61 · 2017: 48 · 2016: 33 · 2015: 23 · 2014: 13 · 2013: 1
- FWCI
- 23.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- 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, knock-in mice, amyloid precursor protein, APP mutations, Swedish mutation, Arctic mutation, amyloid-beta pathology, neuroinflammation
- MeSH terms
- Age Factors, Alzheimer Disease, Analysis of Variance, Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Humans
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