The most significant of these are: (i) the cholinergic hypothesis which postulates that the cognitive decline can be linked to a decrease in the amount of the neurotransmitter acetylcholine (ACh)5 and (ii) the amyloid hypothesis which instead ascribes AD symptoms to the Amyloid Precursor Protein (APP) that undergoes a sequential post-translational proteolysis/processing by β-secretase 1 (BACE-1) and γ-secretase leading to the formation of hydrophobic Aβ peptide fibrils that readily accumulate and deposit on neuritic plaques in the gray matter of the brain.6 This evidence concerns the gene APP and Alzheimer disease.