In an aluminum chloride-induced AD rat model, oral administration of nattokinase not only reduced acetylcholinesterase (AchE) activity, but transformed growth factor-beta (TGF-β), Fas, and interleukin-6 (IL-6) content in the AD pathway and also restored the expression of metalloproteinase domain (9ADAM9) and metalloproteinase domain (10ADAM10) genes [115]. Here, ACHE is linked to Alzheimer disease.