When administered i.p. at a dose of 50 mg/kg to a rat model of streptozotocin (STZ)-induced AD, it provided neuroprotection by activating the α7 nAChR (nicotinic acetylcholine receptor)/NRF2/HO-1 pathway, improving cognitive deficits, and reducing acetylcholinesterase (AChE) activity, Aβ aggregation and mitochondrial toxicity (100). The gene discussed is ACHE; the disease is Alzheimer disease.