Puerarin forms a stable complex with calcium/calmodulin kinase IIα (CaMK IIα), a key protein for synaptic plasticity, which can alleviate the synaptic plasticity damage caused by Alzheimer’s disease through p38MAPK/cAMP-response element binding protein (CREB) signaling pathway (Liu S. et al., 2021) and inhibit the activity of acetylcholinesterase (AChE) in brain tissue. Here, ACHE is linked to early-onset autosomal dominant Alzheimer disease.