“…[36,37] Our earlier study has demonstrated that NRG1 protects the Ab, Swe-APP or C-terminal fragment of APP, which induces cell death and oxidative stress via ErbB4 receptor activation. [27,28] Several studies have demonstrated that ROS are involved in the apoptotic mechanisms that are induced by Ab-mediated neurotoxicity and may, therefore, contribute to the increased apoptosis that is observed in some models of AD. [38,39] Dead neurons in AD may exhibit typical features of apoptosis, such as chromatin condensation and DNA fragmentation.…”