Ferroptosis and neuroinflammation are critical factors in the pathogenesis of central neurological disorders, including neurodegenerative diseases, ischemic stroke, traumatic brain injury, and epilepsy. Ferroptosis, a form of regulated cell death, is triggered by iron overload and reactive oxygen species (ROS), leading to lipid peroxidation and mitochondrial dysfunction. Neuroinflammation, an immune response involving microglia and astrocytes, exacerbates neuronal damage by releasing pro-inflammatory cytokines and chemokines. The interplay between these two processes is essential for understanding the progression of neurological diseases and developing therapeutic strategies. Ferroptosis is regulated by key pathways such as SIRT1, Nrf2, NF-κB, Cox-2, and iNOS/NO. SIRT1 modulates energy metabolism and inflammation, while Nrf2 activates antioxidant pathways to counteract oxidative stress. NF-κB, a central transcription factor, drives neuroinflammation and ferroptosis by regulating inflammatory responses. Cox-2, involved in prostaglandin synthesis, contributes to neuroinflammation and ferroptosis through lipid peroxidation. iNOS/NO, produced by activated microglia, promotes neuroinflammation and may inhibit ferroptosis by suppressing 15-HpETE-PE production. The co-regulation of ferroptosis and neuroinflammation is crucial for cognitive dysfunction and neuronal damage in central nervous system disorders. Understanding the molecular mechanisms, such as the SIRT1/Nrf2/GPX4 pathway, provides potential therapeutic targets for mitigating neuroinflammation and ferroptosis. Research highlights the importance of modulating these pathways to improve outcomes in neurological diseases. The interplay between these processes underscores the need for further investigation into their shared mechanisms and the development of targeted interventions.Ferroptosis and neuroinflammation are critical factors in the pathogenesis of central neurological disorders, including neurodegenerative diseases, ischemic stroke, traumatic brain injury, and epilepsy. Ferroptosis, a form of regulated cell death, is triggered by iron overload and reactive oxygen species (ROS), leading to lipid peroxidation and mitochondrial dysfunction. Neuroinflammation, an immune response involving microglia and astrocytes, exacerbates neuronal damage by releasing pro-inflammatory cytokines and chemokines. The interplay between these two processes is essential for understanding the progression of neurological diseases and developing therapeutic strategies. Ferroptosis is regulated by key pathways such as SIRT1, Nrf2, NF-κB, Cox-2, and iNOS/NO. SIRT1 modulates energy metabolism and inflammation, while Nrf2 activates antioxidant pathways to counteract oxidative stress. NF-κB, a central transcription factor, drives neuroinflammation and ferroptosis by regulating inflammatory responses. Cox-2, involved in prostaglandin synthesis, contributes to neuroinflammation and ferroptosis through lipid peroxidation. iNOS/NO, produced by activated microglia, promotes neuroinflammation and may inhibit ferroptosis by suppressing 15-HpETE-PE production. The co-regulation of ferroptosis and neuroinflammation is crucial for cognitive dysfunction and neuronal damage in central nervous system disorders. Understanding the molecular mechanisms, such as the SIRT1/Nrf2/GPX4 pathway, provides potential therapeutic targets for mitigating neuroinflammation and ferroptosis. Research highlights the importance of modulating these pathways to improve outcomes in neurological diseases. The interplay between these processes underscores the need for further investigation into their shared mechanisms and the development of targeted interventions.