Central neurological disorders, including neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, and depression, are significant contributors to morbidity, mortality, and long-term disability. Ferroptosis and neuroinflammation play pivotal roles in the pathogenesis of cognitive impairment in these disorders. The concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and reactive oxygen species (ROS) has led to a focus on their co-regulatory mechanisms. This paper explores the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, emphasizing the core molecules within shared pathways, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO, and the contributions of different immune cells and structures to cognitive dysfunction. Ferroptosis, a form of regulated cell death triggered by iron overload, involves distinct inducible factors and metabolites. It disrupts cellular REDOX functions and impairs mitochondrial function, leading to neuronal death and cognitive impairment. Neuroinflammation, a defensive immune response, involves the activation of microglia and astrocytes, which release various cytokines and chemokines, exacerbating neuronal damage and cognitive dysfunction. The interplay between ferroptosis and neuroinflammation is highlighted by the shared molecular pathways involving SIRT1, Nrf2, and NF-κB. SIRT1, a histone deacetylase, regulates energy metabolism, inflammation, and cell death pathways. It modulates Nrf2 activity, which activates antioxidant responses and inhibits ferroptosis. Nrf2 also influences NF-κB activity, which triggers pro-inflammatory cytokine release. NF-κB, a transcription factor, regulates neuroinflammation through various pathways, including the NLRP3 inflammasome and STING pathway. Cox-2, an enzyme that produces prostaglandins, is upregulated in neuroinflammation and contributes to lipid peroxidation and neurodegeneration. Its expression is regulated by NF-κB and can be influenced by microRNAs and long non-coding RNAs. iNOS, an enzyme that produces nitric oxide (NO), is associated with neuroinflammation and neuropathic pain. NO can independently regulate ferroptosis and influence the phenotype of microglia and macrophages. The blood–brain barrier (BBB) plays a crucial role in facilitating communication between the brain and external substances. Its impairment is observed in various neurodegenerative diseases, highlighting the importance of understanding its involvement in the pathological processes. Overall, a deeper understanding of the common pathways between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis in central neurological disorders.Central neurological disorders, including neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, and depression, are significant contributors to morbidity, mortality, and long-term disability. Ferroptosis and neuroinflammation play pivotal roles in the pathogenesis of cognitive impairment in these disorders. The concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and reactive oxygen species (ROS) has led to a focus on their co-regulatory mechanisms. This paper explores the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, emphasizing the core molecules within shared pathways, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO, and the contributions of different immune cells and structures to cognitive dysfunction. Ferroptosis, a form of regulated cell death triggered by iron overload, involves distinct inducible factors and metabolites. It disrupts cellular REDOX functions and impairs mitochondrial function, leading to neuronal death and cognitive impairment. Neuroinflammation, a defensive immune response, involves the activation of microglia and astrocytes, which release various cytokines and chemokines, exacerbating neuronal damage and cognitive dysfunction. The interplay between ferroptosis and neuroinflammation is highlighted by the shared molecular pathways involving SIRT1, Nrf2, and NF-κB. SIRT1, a histone deacetylase, regulates energy metabolism, inflammation, and cell death pathways. It modulates Nrf2 activity, which activates antioxidant responses and inhibits ferroptosis. Nrf2 also influences NF-κB activity, which triggers pro-inflammatory cytokine release. NF-κB, a transcription factor, regulates neuroinflammation through various pathways, including the NLRP3 inflammasome and STING pathway. Cox-2, an enzyme that produces prostaglandins, is upregulated in neuroinflammation and contributes to lipid peroxidation and neurodegeneration. Its expression is regulated by NF-κB and can be influenced by microRNAs and long non-coding RNAs. iNOS, an enzyme that produces nitric oxide (NO), is associated with neuroinflammation and neuropathic pain. NO can independently regulate ferroptosis and influence the phenotype of microglia and macrophages. The blood–brain barrier (BBB) plays a crucial role in facilitating communication between the brain and external substances. Its impairment is observed in various neurodegenerative diseases, highlighting the importance of understanding its involvement in the pathological processes. Overall, a deeper understanding of the common pathways between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis in central neurological disorders.