The results of behavioural and pharmacological experiments indicated that PRE treatment remarkably ameliorated the impairment of learning and memory in AD model mice, and significantly reduced the levels of amyloid‐β (Aβ) plaques (Figure S2) and Aβ1–42 monomers, and increased the levels of acetylcholine and brain‐derived neurotrophic factor in the cerebral cortex (Ccx) and hippocampus (Hp) of AD mice (Figure S3) (see the Supporting Information for details). The gene discussed is BDNF; the disease is Alzheimer disease.