Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
Open accessAbstract
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 human Alzheimer's disease and mouse Aβ amyloidosis models.
“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]
The Amyloid-associated neuroinflammation and pathology section and Fig. 4 caption report activated, hypertrophic microglia clustered around amyloid plaques in APPPS1-21 mice (page not provided). The paper compares mouse plaque appearance with human AD plaques, but the passages do not establish that activated microglia surround plaques in human patients. (LLM, conf=0.88)
Experimental — accuracy not yet measuredA previous report found no sex-dependent differences in Aβ accumulation in the APPPS1-21 mouse model.
“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]
The Cerebral amyloidosis section reports that male and female APPPS1-21 mice did not differ statistically in Aβ levels or amyloid load at 1–2 months of age. The sex comparison was limited to those early ages, so it does not establish an absence of sex-dependent differences in Aβ accumulation generally. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThere is no sex-dependent difference in the phenotypes of APP(Swe)/PS1(L166P) mice.
“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]
The Cerebral amyloidosis section reports that Aβ levels and amyloid load in 1- and 2-month-old male APPPS1-21 mice were not statistically different from females. That supports no sex difference in those measured early amyloid outcomes, but the paper says the analysis was mainly restricted to females and does not establish no sex-dependent difference across the mice’s phenotypes. (LLM, conf=0.88)
Experimental — accuracy not yet measuredReactive gliosis, encompassing microgliosis and astrogliosis, are prevalent neuropathological hallmarks in the brains of both human AD and mouse models of Aβ amyloidosis.
“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]
The ‘Amyloid-associated neuroinflammation and pathology’ section reports microgliosis and simultaneous astrocytosis after plaques appeared in APPPS1-21 mice. The paper does not establish that both are prevalent hallmarks in human AD brains, so the human part of the attributed claim is unsupported by this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThere is no sex effect in the APP/PS1 experimental group.
“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]
The Cerebral amyloidosis section reports that Aβ levels and amyloid load in male APPPS1-21 mice at 1–2 months were not statistically different from those in females. That supports a lack of detected sex difference for those measures and ages, but not the broader assertion that there is no sex effect in the experimental group generally. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Sample sizes were justified by prior publications using APP/PS1 and P301S mouse models that provided estimates of expected effect sizes and variance.
“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
The Cerebral amyloidosis results and Fig. 6 report APPPS1-21 outcomes, sample sizes, and measures of variability that could inform estimates for that model. The paper does not study P301S mice or state that its results were used to choose the citing study’s sample sizes. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAPPPS1 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.
“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]
The Introduction and mouse-generation methods identify line 21 as coexpressing APP and PS1-L166P under Thy1 promoter control. They specify the APP mutation as KM670/671NL, not the citing sentence’s K670M/N671L; that mutation designation is not supported. Page numbers are unavailable in our copy. (LLM, conf=0.91)
Experimental — accuracy not yet measuredAPPPS1 mice exhibit early and robust Aβ deposition beginning at 6-8 weeks of age in the cortex and 3-4 months of age in the hippocampus.
“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]
The Introduction identifies the APP and PS1 mutations and neuron-specific Thy1 promoter, and the Cerebral amyloidosis section reports the first neocortical plaques at 6 weeks. The hippocampal timing is less accurate: that section says deposition began in the dentate gyrus at 2–3 months and in CA1 at 4–5 months, rather than beginning throughout the hippocampus at 3–4 months. (LLM, conf=0.88)
Experimental — accuracy not yet measuredDozens of mouse lines overexpressing several combinations of APP and PSEN1 mutations have been created to accelerate the onset of Aβ pathologies in brains.
“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]
The Introduction describes the creation of mice coexpressing mutated APP and PS1, and the Discussion reports earlier amyloid deposition in this model than in other transgenic models. The paper also mentions several APP and APP/PS1 lines, but it does not establish that dozens of lines with several mutation combinations were created. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe APPPS1-21 model begins Aβ accumulation in the neocortex at about 6 to 8 weeks and shows robust Aβ accumulation and plaque deposition at 4 months.
“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]
Abnormal activation of microglia and astrocytes occurs in Alzheimer's disease patients and APPPS1-21 transgenic model mice.
“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]
Amyloid-associated gliosis is consistently observed in the brains of AD patients and amyloidosis mouse models.
“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]
APPPS1-21 mice overexpress a human APP with the Swedish mutation (KM670/671NL) and mutant PS1 with the L166P mutation.
“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
Another study using the APP/PS1 model proposed that the protective variant reduced the number of plaques and overall plaque load.
“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 <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 Radde et al. 2006
The APPPS1 model exhibits rapid deposition of primarily Aβ42.
“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]
The APP/PS1 and APP23 mouse models used in that study express mutated PS1 and/or APP under the neuron-specific Thy1 promoter.
“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]
While some of these mouse models showed evidence of localized hyperphosphorylated tau that may represent 'pretangles', none developed neurofibrillary tangles.
“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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“APOE knock-in and APPPS1-23 mice breeding pairs were gifts from Dr. Patrick Sullivan (Duke University, Durham, NC) and Dr. Mathias Jucker (University of Tübingen, Tübingen, Germany), respectively.”
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- 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
- 31
- 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
- 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
- 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
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 ›
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