ANP32A and Alzheimer disease: To gain insight into the mechanisms underlying the increased ANP32A in AD, HEK293 cells were transiently transfected with pIRES-eGFP-Tau40 or its vector pIRES-eGFP plasmid (Fig. 7a), treated with Aβ oligomers (Fig. 7b) or hydrogen peroxide (H2O2) (Fig. 7c), the recognized precipitating factors of AD [19, 20].