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Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
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We have generated a novel transgenic mouse model on a C57BL/6J genetic background that coexpresses KM670/671NL mutated amyloid precursor protein and L166P mutated presenilin 1 under the control of a neuron-specific Thy1 promoter element (APPPS1 mice). Cerebral amyloidosis starts at 6-8 weeks and the ratio of human amyloid (A)beta42 to Abeta40 is 1.5 and 5 in pre-depositing and amyloid-depositing mice, respectively. Consistent with this ratio, extensive congophilic parenchymal amyloid but minimal amyloid angiopathy is observed. Amyloid-associated pathologies include dystrophic synaptic boutons, hyperphosphorylated tau-positive neuritic structures and robust gliosis, with neocortical microglia number increasing threefold from 1 to 8 months of age. Global neocortical neuron loss is not apparent up to 8 months of age, but local neuron loss in the dentate gyrus is observed. Because of the early onset of amyloid lesions, the defined genetic background of the model and the facile breeding characteristics, APPPS1 mice are well suited for studying therapeutic strategies and the pathomechanism of amyloidosis by cross-breeding to other genetically engineered mouse models.
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“Activated microglia surround amyloid plaques in the brains of both human patients with AD and mouse models of Aβ amyloidosis13,15,21,22.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“although a previous report demonstrated no sex-dependent differences in Aβ accumulation in this APPPS1–21 mouse model13”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“A previous report demonstrated no sex-dependent difference in the phenotypes of APP(Swe)/PS1(L166P) mice8.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [8]
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“The reactive gliosis, encompassing microgliosis and astrogliosis, are prevalent neuropathological hallmarks observed in the brains of both human AD and mouse models of Aβ amyloidosis8,15,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [8]
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“Because it has been known that there is no sex effect in this experimental group8, male and female mice were combined for statistical analyses.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [8]
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“Sample sizes were chosen based on prior publications using the APP/PS1 and P301S mouse models, which provided estimations of expected effect sizes and variance.”
From APOE4 impairs the microglial response in Alzheimer’s disease by inducing TGFβ-mediated checkpoints (2023) · cites this paper as Radde et al., 2006
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“The APPPS1-21 (APPPS1) mouse line coexpresses human amyloid precursor protein harboring the K670M/ N671L familial AD mutation and presenilin 1 harboring the L166P familial AD mutation, under the control of the neuron-specific Thy1 promoter.21”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [21]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“APPPS1 mouse line coexpresses APP K670M/N671L and PS1 L166P mutations under the control of the neuronspecific Thy1 promoter and exhibits early and robust A deposition beginning at 6 -8 weeks of age in the cortex and 3-4 months of age in the hippocampus.21”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [21]
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“dozens of mouse lines overexpressing several combinations of APP and PSEN1 mutations have been created to accelerate the onset of Aβ pathologies in brains [28–30].”
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 [30]
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“The APPPS1–21 mouse model used in our study starts to accumulate Aβ in the neocortex at approximately 6 to 8 weeks of age and exhibits robust Aβ accumulation and plaque deposition at 4 months of age13.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [13]
The cited source says what the claim attributes to it.
In the citing paper
“Abnormal activation of microglia and astrocytes is observed in the brains of AD patients15 and APPPS1–21 transgenic model mice13.”
From Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models (2026) · cites this paper as [13]
The cited source says what the claim attributes to it.
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“Amyloid-associated gliosis is consistently observed in the brains of AD patients15 and amyloidosis mouse models8,16.”
From Effects of SPI1-mediated transcriptome remodeling on Alzheimer's disease-related phenotypes in mouse models of Aβ amyloidosis (2024) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“APPPS1-21 mice overexpress a human APP with a Swedish mutation (KM670/671NL) and mutant PS1 with the L166P mutation.”
From Haploinsufficiency of Human APOE Reduces Amyloid Deposition in a Mouse Model of Amyloid-β Amyloidosis (2011) · cites this paper as Radde et al., 2006
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In the citing paper
“During submission of this manuscript, another study (Takalo et al. 2025), using the APP/PS1 model which develops an elevated Aβ42:40 (~5:1) (Radde et al. 2006), proposed that the protective variant reduced the number of plaques and overall plaque load”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Radde et al. 2006
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In the citing paper
“we mated Cx3cr1 knockout mice to two different mouse models of AD that exhibit either rapid deposition of primarily A42 (the APPPS1 model) 21 or gradual deposition of primarily A40 (the R1.40 model).[22][23][24]”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [21]
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“The increased levels of CH25H mRNA and protein were also observed in the frontal cortex of 4-month-old APPPS1-21 mice bearing amyloid plaques [65] (Fig. 1c, d, e).”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [65]
In the citing paper
“the study utilized APP/PS1 and APP23 transgenic mouse models, both of which were generated through expression of mutated PS1 and/or APP under the neuron-specific Thy1 promoter element [151, 152].”
From Microglial dysfunction in brain aging and Alzheimer's disease (2014) · cites this paper as [151]
In the citing paper
“The other major limitation of these mouse models was that while some showed evidence of localized hyperphosphylated tau that may represent “pretangles”[107, 118, 151, 159], none developed neurofibrillary tangles.”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [118]
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Metadata
- Authors
- Radde, R., Bolmont, T., Kaeser, S. A., Coomaraswamy, J., Lindau, D., Stoltze, L., Calhoun, M. E., Jäggi, F., Wolburg, H., Gengler, S., Haass, C., Ghetti, B., Czech, C., Hölscher, C., Mathews, P. M., & Jucker, M.
- Affiliations
- Hertie Institute for Clinical Brain Research (DE)
- University of Basel (CH)
- University of Tübingen (DE)
- University of Ulster (GB)
- Adolf-Butenandt-Institut für Physiologische Chemie, Physikalische Biochemie und Zellbiologie (DE)
- Indiana University School of Medicine (US)
- F. Hoffmann-La Roche AG (CH)
- New York University (US)
- Corresponding author
- Jucker, Mathias
- ORCID
- Venue
- The EMBO Reports
- Published
- 2006-08-11
- Volume
- 7
- Issue
- 9
- Pages
- 940-946
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC1559665
- OpenAlex
- W2156788921
- Cited by
- 986
- References
- 32
- Citations by year
- 2026: 33 · 2025: 60 · 2024: 75 · 2023: 85 · 2022: 73 · 2021: 86 · 2020: 93 · 2019: 79 · 2018: 58 · 2017: 41 · 2016: 46 · 2015: 41 · 2014: 36 · 2013: 50 · 2012: 37
- FWCI
- 9.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- EMBO Reports (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- European Commission (LSHM-CT-2003-503330)
- Boehringer Ingelheim Stiftung
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- cerebral amyloidosis, amyloid-beta 42, amyloid angiopathy, tau hyperphosphorylation, gliosis, microglia, Alzheimer's disease model
- MeSH terms
- Animals, Cognition, Disease Models, Animal, Inflammation, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Peptide Fragments, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Cerebral Amyloid Angiopathy, Neocortex, Mice, Presenilin-1
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