The cholinesterase inhibitors that interact simultaneously with AChE (catalytic and peripheral sites) and Aβ plaque deposition coupled with added properties such as antioxidant action [122], neuroprotective or voltage-dependent calcium channel antagonistic activity [123,124,125,126], histamine H3 receptor antagonism [127,128,129,130], cannabinoid CB1 receptor antagonism [131,132], and beta-site APP cleaving enzyme (BACE1) inhibition [70,125,133,134] display the potential of ameliorating the cognitive deficit in AD by restoring cholinergic activities [135,136,137]. The gene discussed is BACE1; the disease is Alzheimer disease.