APP and Alzheimer disease: However, these transcriptome data were generated from ‘middle-aged’ (12 months old) mice rather than young adults, and the endogenous App gene of the mouse was altered with a total of six mutations (three that humanise the sequence of the Aβ region and three EOFAD mutations), motivated by the idea that the more aggregation-prone human Aβ sequence plays a critical role in the pathogenic mechanism of AD.