Increased BChE activity7 in addition to reduced expression of neuronal AChE in advanced AD9, findings that AChE knockout mice are viable and develop a primitive cholinergic neuronal network with BChE acting as a surrogate for AChE and taking over the hydrolysis of ACh in the brain17, along with the fact that BChE knockout mice show no physiological disadvantages18, have led to the hypothesis that BChE takes over the ChE activity in advanced AD, and thus needs to be inhibited to restore the brain levels of ACh17. This evidence concerns the gene ACHE and Alzheimer disease.