According to the “amyloid hypothesis”, genetic and environmental factors result in altered processing of APP, accumulation of intracellular amyloid-beta peptides (Aβ) and the microtubule protein tau, imbalance between production, degradation, and clearance of Aβ leading to accumulation of extracellular Aβ, activation of microglia and astrocytes, and a cascade of events resulting in inflammation, synapse dysfunction, neuronal loss, and cognitive decline [2–5]. The gene discussed is APP; the disease is Mental deterioration.