In AD, there are two well-described processes, namely, (1) the formation of Aβ senile plaques, through an imbalance in the processing of APP (see Table 1), and APP processing appears to be an initiating factor for AD [29], (2) the formation of neurofibrillary tangles (NFTs) through pathological processing of tau involving phosphorylations and protease cleavage, and subsequent aggregation [28], a process that appears to be directly involved in triggering neuronal death [30, 31]. This evidence concerns the gene APP and Alzheimer disease.