To halt AD progression, therapeutic agents may need to target the different underlying causes of the disease, including the accumulation of extracellular amyloid β (Aβ) plaques, intracellular tau neurofibrillary tangles, oxidative stress, inflammatory processes, metabolic abnormalities, impaired growth factors, synaptic dysfunction, neural loss, and particularly the inhibition of acetylcholinesterase [7,8]. Here, ACHE is linked to Alzheimer disease.