Increase in Tau Pathology in P290S Mapt Knock-In Mice Crossed with App NL-G-F Mice
Open accessAbstract
Alzheimer’s Disease (AD) is characterized by the pathologic assembly of amyloid β (Aβ) peptide, which deposits into extracellular plaques, and tau, which accumulates in intraneuronal inclusions. To investigate the link between Aβ and tau pathologies, experimental models featuring both pathologies are needed. We developed a mouse model featuring both tau and Aβ pathologies by knocking the P290S mutation into murine Mapt and crossing these Mapt P290S knock-in (KI) mice with the App NL-G-F KI line. Mapt P290S KI mice developed a small number of tau inclusions, which increased with age. The amount of tau pathology was significantly larger in App NL-G-F xMapt P290S KI mice from 18 months of age onward. Tau pathology was higher in limbic areas, including hippocampus, amygdala, and piriform/entorhinal cortex. We also observed AT100-positive and Gallyas-Braak-silver-positive dystrophic neurites containing assembled filamentous tau, as visualized by in situ electron microscopy. Using a cell-based tau seeding assay, we showed that Sarkosyl-insoluble brain extracts from both 18-month-old Mapt P290S KI and App NL-G-F xMapt P290S KI mice were seed competent, with brain extracts from double-KI mice seeding significantly more than those from the Mapt P290S KI mice. Finally, we showed that App NL-G-F xMapt P290S KI mice had neurodegeneration in the piriform cortex from 18 months of age. We suggest that App NL-G-F xMapt P290S KI mice provide a good model for studying the interactions of aggregation-prone tau, Aβ, neuritic plaques, neurodegeneration, and aging.
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The results are consistent with those recently reported for an APPNL-G-F/MAPTP290S mouse.
“These results are consistent with those recently reported for an APPNL-G-F/MAPTP290S mouse, which is a mouse model in which both human APP and human MAPT are knockins (Huang 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 Huang et al., 2022
The Abstract and Materials and Methods (Mouse lines; page not provided) identify the APPNL-G-F × MaptP290S mouse and report increased tau pathology, supporting the citation’s identification of the model. But Mouse lines says the P290S mutation was inserted into murine Mapt and describes the APP line as expressing humanized Aβ; it does not support the statement that both human APP and human MAPT were knocked in. The citing paper’s own results are not provided, so their consistency with Huang et al.’s findings cannot be assessed here. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe report on the APPNL-G-F/MAPTP290S mouse showed enhancement of MAPT pathology by Aβ but the pathology occurs only in very old mice, and the manuscript did not provide information on other pathologies such as inflammation or m6A.
“The report on the APPNL-G-F/MAPTP290S mouse showed enhancement of MAPT pathology by Aβ but the pathology occurs only in very old mice, and the manuscript did not provide any information on other pathologies, such as inflammation or m6A.”
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 Huang et al., 2022
The Discussion (page unavailable) says Aβ significantly increased tau inclusions only from 18 months of age, although some tau inclusions occurred earlier. The Results section on age-dependent neurodegeneration reports nerve-cell loss in the double-knock-in mice from 18 months, so the claim that the paper provided no information on other pathologies is too broad. The passages found do not report inflammation or m6A findings. (LLM, conf=0.88)
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- Authors
- Huang, M., Macdonald, J., Lavenir, I., Chen, R., Craxton, M., Slavik-Smith, E., Davies, S. W., & Goedert, M.
- Affiliations
- MRC Laboratory of Molecular Biology (GB)
- University College London (GB)
- Corresponding author
- Davies, Stephen W.
- Venue
- eneuro
- Publisher
- Society for Neuroscience
- Published
- 2022-11
- Volume
- 9
- Issue
- 6
- Pages
- ENEURO.0247-22.2022
- ISSN
- 2373-2822 (ISSN-L)
- PMC
- PMC9770019
- OpenAlex
- W4311704493
- Cited by
- 19
- References
- 39
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 6 · 2023: 4
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- eNeuro (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Apollo (cc-by)
- Funders
- UK Dementia Research Institute
- 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, tau pathology, amyloid-beta, tau seeding, dystrophic neurites, neurodegeneration, piriform cortex, limbic system, aging, amyloid plaques
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Mice, Transgenic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Mice, Plaque, Amyloid
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