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80 This reduction may be attributed to impaired TLR4 and PPAR-γ signaling
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1 Introduction Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, memory loss, and neuropsychiatric symptoms, representing one of the most critical global public health challenges of the 21st century ( In this context, ferroptosis—a newly defined, regulated cell death modality driven by iron-dependent lipid peroxidation—has rapidly emerged as a frontier and focus in AD research ( Ferroptosis, a regulated form of cell death, plays a significant role in various pathological conditions, including neurodegeneration, cancer, and ischemia–reperfusion injury ( Figure 1 ) ( Figure 1 This review aims to systematically elucidate the central role of iron dyshomeostasis and the ferroptosis process it drives in the pathogenesis of Alzheimer’s disease
