Using this model as a base, we could study the potential mechanisms that may be involved in the development of AD and its corresponding sequelae, which comprise Aβ accumulation, the expression of p-tau, NFL and GFAp, microvascular injury, genetic factors like the pathway of the APOE ε4, neuroinflammation (signatures such as cytokines of IL-6, IL-1, and Gal-3), and microglial activation [107,108,109,110,111,112]. This evidence concerns the gene IL1B and Alzheimer disease.