Endoplasmic reticulum stress (ERS) regulates the expression and activity of beta-site APP-cleaving enzyme 1 (BACE1) at multiple levels including transcription, translation and post-translation by activating the unfolded protein response pathway. This will further alleviate the pathological process of Aβ in Alzheimer's disease. The PERK-eIF2α-ATF4 axis is the key mechanism by which ERS upregulates BACE1. Continuous ERS could prompt PERK to phosphorylate eIF2α, which directly binds to the BACE1 promoter, increasing its transcriptional and protein levels and accelerating amyloid protein production. On the other hand, the IRE1- XBP1s and ATF6 pathways promote the degradation of BACE1 and APP non-amyloidogenic pathway cleavage by upregulating ERAD key factors in early ERS, which has an inhibitory effect on Aβ production. Therefore, the regulation of BACE1 by ERS is bidirectional through the PERK, IRE1 or ATF6 pathways. This article summarized the research progress of the relevant mechanisms, with the aim of seeking new strategies to restore protein homeostasis and slow down the pathological process of AD through intervention targeting ERS.