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The potential molecular mechanisms underlying these effects included disturbances in redox homeostasis (as evidence by the enhanced production of ROS and reactive nitrogen species), failure of enzymatic and nonenzymatic cytoprotective mechanisms involving the glutathione system as well as nuclear factor kappa B (NF-B) and fibroblast growth factor 2-mediated pathways, and impaired mitochondrial function

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Inhibiting ferroptosis via iron chelators, radical-trapping agents, and other interventions demonstrates significant improvements in neuronal survival and synaptic function across diverse preclinical models, establishing ferroptosis targeting as a promising novel therapeutic strategy for AD

Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections, 421, 241243