In order to investigate the prospective therapeutic value of pinocembrin on cognitive impairment and neuronal apoptosis in correlation with neurodegeneration in AD, Aβ neurotoxicity induced learning and memory deficits and neuronal injury were established by a single intracerebroventricular infusion of Aβ25-35, an Aβ1-42-treated RAGE overexpressing cell model, and a copper-treated APPsw overexpressing cell system, all of which could well reflect Aβ toxicity in an Aβ-rich environment both in vivo and in vitro. This evidence concerns the gene AGER and Alzheimer disease.