BACE1 and Alzheimer disease: Bahn et al. revealed a previously unknown molecular mechanism, in which Nrf2-deficient AD mice had significantly increased BACE1 and BACE1-AS expression and Aβ deposition, and more severe cognitive dysfunction compared with 5xFAD and Nrf2 knockout mice, whereas the activation of Nrf2 inhibited BACE1 and BACE1-AS expression and Aβ production and improved cognitive dysfunction and AD-related pathological characteristics (Bahn et al., 2019).