APP and Alzheimer disease: In addition, injection of double selenium nanospheres (CLNDSe) in an AD mouse model revealed abnormal microglia protofibrils or tau protein-targeted aggregation outside of Aβ42, and its crossing of the BBB into the brain significantly downregulated ROS, ACSL4, and COX-2, and upregulated FTH1, GPX1, and GPX4, ultimately inhibiting ferroptosis and ameliorating cognitive deficits in APP/PS1 mice (Solovyev et al., 2018).