The most well-known pathological features of AD are the accumulation of amyloid-beta (Aβ) plaques composed of a cleaved fragment of amyloid precursor protein (APP) and hyperphosphorylated tau (pTau) tangles, which are believed to synergistically contribute to synaptic dysfunction, neuron death, and cognitive decline (Mattson, 2004; Soria-Lopezet al, 2019). This evidence concerns the gene APP and Alzheimer disease.