Moreover, in the Aβ1–42 mouse model of Alzheimer’s disease, they may enhance the ability of anthocyanins (12 μg/g) to ameliorate memory impairment, as well as protect their pre- and postsynaptic proteins from Aβ1–42-induced synaptic dysfunction, regulate the p-PI3K/p-Akt/p-GSK3β pathway, prevent the hyperphosphorylation of tau protein at serines 413 and 404, and inhibit apoptosis during 14 days of treatment [211]. Here, GSK3B is linked to Alzheimer disease.