The mechanisms of cholinesterase inhibitors (ChEIs)—as standard therapeutic agents for AD and vascular dementia—are generally characterized on the basis of their structural properties [96,97]; for example, effectively blocking the degradation of synaptic gap ACh through selective inhibition of AChE and butyrylcholinesterase (BuChE) (inhibition constants Ki of 0.13–14.74 nM and 5.11–23.95 nM, respectively), thus improving cholinergic neurotransmission. The gene discussed is ACHE; the disease is Alzheimer disease.