APP and Alzheimer disease: At the animal experimental level, by over-expressing SGK1 in the hippocampus of a female middle-aged APP/ PS1 mouse model, it was found that SGK1 over-expression significantly increased the level of hippocampal IDE (enzyme for degrading Aβ), which significantly reversed the spatial memory impairment caused by AD, and at the same time, SGK1 overexpression promotes the increase of non-amyloid metabolism and degradation of Aβ induced by APP, leading to a decrease in the production and deposition of Aβ (Lian et al., 2020).