Article
A third-generation mouse model of Alzheimer's disease shows early and increased cored plaque pathology composed of wild-type human amyloid β peptide.
The Journal of biological chemistry - 1 Sept 2021
Sato Kaori, Watamura Naoto, Fujioka Ryo, Mihira Naomi, Sekiguchi Misaki, Nagata Kenichi, Ohshima Toshio, Saito Takashi, Saido Takaomi C, Sasaguri Hiroki
Abstract excerpt
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 (AppNL-G-F and AppNL-F mice, respectively). These models showed Aβ pathology, neuroinflammation, and cognitive impairment in an age-dependent manner. The former model exhibits extensive pathology as early as 6 months, but is unsuitable for...
Topics
- Alzheimer Disease
- Amyloid beta-Peptides
- Animals
- Disease Models, Animal
- Gene Knock-In Techniques
- Humans
- Mice
- Mice, Transgenic
- Mutation
- Plaque, Amyloid