ACHE and Alzheimer disease: In contrast, BuChE function increases while AChE activity either stabilises or decreases in AD patients' central nervous systems.5 The cholinergic shortage assumed to be the leading cause of the deficiencies in cognitive, behavioral, and general functioning that are characteristic of AD can therefore be addressed by targeting these enzymes as potential therapeutic targets.6 Since 2003, no brand-new treatments for AD have been approved by the FDA.7 BuChE has been linked to AD and reported to have a major pharmaceutical target function.