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• W4311704493 endingPage "22.2022" @default.
• W4311704493 startingPage "ENEURO.0247" @default.
• W4311704493 abstract "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 MaptP290S knock-in (KI) mice with the AppNL-G-F KI line. MaptP290S KI mice developed a small number of tau inclusions, which increased with age. The amount of tau pathology was significantly larger in AppNL-G-FxMaptP290S 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 MaptP290S KI and AppNL-G-FxMaptP290S KI mice were seed competent, with brain extracts from double-KI mice seeding significantly more than those from the MaptP290S KI mice. Finally, we showed that AppNL-G-FxMaptP290S KI mice had neurodegeneration in the piriform cortex from 18 months of age. We suggest that AppNL-G-FxMaptP290S KI mice provide a good model for studying the interactions of aggregation-prone tau, Aβ, neuritic plaques, neurodegeneration, and aging." @default.
• W4311704493 created "2022-12-28" @default.
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• W4311704493 date "2022-11-01" @default.
• W4311704493 modified "2023-10-10" @default.
• W4311704493 title "Increase in Tau Pathology in P290S<i>Mapt</i>Knock-In Mice Crossed with<i>App</i>^NL-G-FMice" @default.
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• W4311704493 doi "https://doi.org/10.1523/eneuro.0247-22.2022" @default.
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