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- W3157697954 abstract "Abstract We previously developed single App knock-in mouse models of Alzheimer’s disease (AD), harboring the Swedish and Beyreuther/Iberian mutations with or without the Arctic mutation ( App NL-G-F and App NL-F mice). These models showed amyloid β peptide (Aβ) pathology, neuroinflammation and cognitive impairment in an age-dependent manner. The former line exhibits extensive pathology as early as 6 months but is unsuitable for investigating Aβ metabolism and clearance because the Arctic mutation renders Aβ resistant to proteolytic degradation and prone to aggregation. In particular, it is inapplicable to preclinical immunotherapy studies due to its discrete affinity for anti-Aβ antibodies. The weakness of the latter model is that it may take as long as 18 months for the pathology to become prominent. We have thus generated a new model that exhibits early deposition of wild-type human Aβ by crossbreeding the App NL-F line with the Psen1 P117L/WT line. We show that the effects of the pathogenic mutations in the App and Psen1 genes are additive or synergistic. This new mouse model showed more cored plaque pathology and neuroinflammation than App NL-G-F mice and will help accelerate the development of disease-modifying therapies to treat preclinical AD." @default.
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- W3157697954 date "2021-04-30" @default.
- W3157697954 modified "2023-09-27" @default.
- W3157697954 title "New App knock-in mice that accumulate wild-type human Aβ as rapidly as AppNL-G-F mice exhibit intensive cored plaque pathology and neuroinflammation" @default.
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- W3157697954 doi "https://doi.org/10.1101/2021.04.30.442122" @default.
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