It also downregulated the expression of cyclooxygenase-2 (COX-2) and cysteine-3 (C3) to exert anti-Alzheimer’s disease effects (Liu et al., 2019) and decreased cognitive deficits in lead acetate-induced neurotoxicity mice by elevating the activities of acetylcholinesterase (AChE) and monoamine oxidase (MAO) and modulating the PKA/Akt/NOS signaling pathway (Liu et al., 2013). The gene discussed is ACHE; the disease is Alzheimer disease.