Increased BACE1-AS and BACE1 expression, Aβ deposition and cognitive deficits were more pronounced in Nrf2-deficient AD mice compared with Nrf2-deficient mice and AD mice, suggesting that Nrf2 is a negative regulator of BACE1-AS and BACE1 (Bahn et al. 2019). Here, BACE1 is linked to Alzheimer disease.