These interventions directly target acetylcholinesterase (AChE), Aβ peptide, or tau proteins [8-12] and/or modulate the signaling pathways underlying Aβ oligomer formation, tau hyperphosphorylation, or other AD-related pathologies, such as inflammation, oxidative stress and impaired adult neurogenesis [12-16]. This evidence concerns the gene ACHE and Alzheimer disease.