Results indicated that the neuroprotective effects of WA in AD are mediated by its ability to reduce beta-amyloid plaque aggregation, tau protein accumulation, inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities, regulation of heat shock proteins, and inhibition of oxidative and inflammatory components. This evidence concerns the gene ACHE and Alzheimer disease.