To conclude, the present study has amply demonstrated that PA could ameliorate the cognitive deficits in TgCRND8 mice via suppressing Aβ plaques deposition, the hyperphosphorylation of tau protein, neuroinflammation and gut dysbiosis through inhibiting the activation of C/EBPβ/AEP pathway (Fig. 8), suggesting that PA is a potential candidate worthy of further development into the pharmaceutical treatment of AD. Here, CEBPB is linked to Alzheimer disease.