As a result of the so-called ‘cholinergic hypothesis’, up to date, the pharmacological therapy of AD has essentially been based on the restoration of adequate levels of acetylcholine (ACh) ensured by acetylcholinesterase (AChE) inhibitors (i.e., rivastigmine, galantamine, and donepezil) [2], but also butyrylcholinesterase (BChE) inhibitors. Here, ACHE is linked to Alzheimer disease.