The existing clinical therapies for symptomatic treatment of AD, including acetylcholinesterase (AChE) inhibitors, lack the disease-modifying potential and are associated with several side effects, such as cardiovascular and gastrointestinal adverse effects, resulting from overstimulation of peripheral cholinergic activity (Schneider 2000; Ruangritchankul et al. 2021). This evidence concerns the gene ACHE and Alzheimer disease.