Many mouse models of Alzheimer's disease (AD) rely on overexpression of amyloid precursor (APP) transgenes, which makes it difficult to tease out which effects are truly disease-relevant and which are induced by the overexpression. In this study, the authors describe several new knock-in AD model mice that express mutant APP at near physiological levels.
- Takashi Saito
- Yukio Matsuba
- Takaomi C Saido