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Se alleviates cerebral ischemia-induced neurological damage by activating GPX4 in IS ( (CLNDSe) in an AD mouse model revealed abnormal microglia protofibrils or tau protein-targeted aggregation outside of A42, 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)

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