It assumes that, in the early stage of AD, the brain has low levels of choline acetyltransferase, and cholinergic neurons involved in the synthesis of acetylcholine lose their function, resulting in cognitive dysfunction.4,24 Thus, a widely studied therapeutic strategy in AD is to increase cholinergic levels in the brain by inhibiting its degradation using AChE inhibitors.25,26 However, the cholinergic hypothesis has been questioned, since AChE inhibitors do not stop AD’s progression, providing only relief of cognitive symptoms.4,25. The gene discussed is ACHE; the disease is Alzheimer disease.