Bacteria-derived equol alleviates Aβ toxicity in C. elegans through PEK-1-associated UPRer activation.

Alzheimer's disease (AD) is the leading cause of dementia with no effective disease-modifying treatments. Here, we found that Escherichia coli (E. coli) DH5α relieved learning defects and paralysis, and prolonged lifespan in amyloid-β (Aβ)-expressing C. elegans. DH5α inhibited Aβ aggregation via activating the PEK-1-dependent endoplasmic reticulum unfolded protein response (UPRer). We further identified equol from DH5α metabolites, which alleviated AD-related phenotypes through the same PEK-1/UPRer pathway.