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Ferroptosis in Neurological Diseases: Moving Towards Therapeutic Intervention

Recent advances have clarified how ferroptosis—a regulated, iron‑dependent form of lipid peroxidation—contributes to a spectrum of neurological disorders, including ischemic stroke, Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Mechanistic studies highlight the central roles of glutathione peroxidase 4 (GPX4), ferroptosis suppressor protein 1 (FSP1), and dihydroorotate dehydrogenase (DHODH) in protecting neurons, while dysregulated iron handling and polyunsaturated fatty‑acid metabolism exacerbate cell death. Pre‑clinical models demonstrate that pharmacologic agents such as selenium compounds, N‑acetylcysteine, ebselen, and vitamin E analogues can mitigate ferroptotic damage, prompting early‑phase clinical trials focused on iron chelation and antioxidant strategies. Collectively, these findings move ferroptosis from a molecular curiosity toward a viable therapeutic target in neurodegeneration.