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Neuroprotective mechanisms function through three processes which include 3-hydroxyhericenone F, which protects against ER stress-induced neuronal death, and 3-hydroxyhericenone F and EB-plaque reduction and gliosis and neuroinflammation in AD research models and 3-hydroxyhericenone F which protects against apoptosis while protecting pro-survival pathways (Roda et al., 2021

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A previous study reported that ferroptosis is most prominent during reperfusion, as interventions targeting ferroptosis primarily reduce reperfusion-related damage but do not significantly affect ischemia-related injury (74)