This review article explores the role of Nrf2 in regulating ferroptosis and its implications for neurodegenerative diseases (NDs). Ferroptosis is an iron-dependent form of lipid peroxidation-induced programmed cell death, closely associated with NDs such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). Accumulating evidence links ferroptosis to the pathogenesis of NDs, with factors such as antioxidant system damage, excessive oxidative stress (OS), and altered Nrf2 expression levels playing key roles. Nrf2 regulates the transcription of anti-ferroptosis systems, including crucial signaling molecules involved in lipid peroxidation and iron metabolism. The regulation of Nrf2 is critical for detecting and treating ferroptosis-related neuronal loss and mitochondrial dysfunction. The article discusses the mechanisms of ferroptosis, including iron metabolism, lipid peroxidation, and the antioxidant system, and highlights the role of Nrf2 in these processes. It also explores the implications of Nrf2 regulation in the diagnosis and treatment of NDs, emphasizing the potential of Nrf2 as a therapeutic target. The review concludes that understanding the relationship between Nrf2 and ferroptosis is essential for developing effective strategies to combat NDs.This review article explores the role of Nrf2 in regulating ferroptosis and its implications for neurodegenerative diseases (NDs). Ferroptosis is an iron-dependent form of lipid peroxidation-induced programmed cell death, closely associated with NDs such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). Accumulating evidence links ferroptosis to the pathogenesis of NDs, with factors such as antioxidant system damage, excessive oxidative stress (OS), and altered Nrf2 expression levels playing key roles. Nrf2 regulates the transcription of anti-ferroptosis systems, including crucial signaling molecules involved in lipid peroxidation and iron metabolism. The regulation of Nrf2 is critical for detecting and treating ferroptosis-related neuronal loss and mitochondrial dysfunction. The article discusses the mechanisms of ferroptosis, including iron metabolism, lipid peroxidation, and the antioxidant system, and highlights the role of Nrf2 in these processes. It also explores the implications of Nrf2 regulation in the diagnosis and treatment of NDs, emphasizing the potential of Nrf2 as a therapeutic target. The review concludes that understanding the relationship between Nrf2 and ferroptosis is essential for developing effective strategies to combat NDs.