The COVID-19 pandemic has caused devastating loss of life and a healthcare crisis worldwide. SARS-CoV-2 is the causative pathogen of COVID-19 and is transmitted mainly through the respiratory tract, where the virus infects host cells by binding to the ACE2 receptor. SARS-CoV-2 infection is associated with acute pneumonia, but neuropsychiatric symptoms and different brain injuries are also present. The possible routes by which SARS-CoV-2 invades the brain are unclear, as are the mechanisms underlying brain injuries with the resultant neuropsychiatric symptoms in patients with COVID-19. Ferroptosis is a unique iron-dependent form of non-apoptotic cell death, characterized by lipid peroxidation with high levels of glutathione consumption. Ferroptosis plays a primary role in various acute and chronic brain diseases, but to date, ferroptosis in COVID-19-related brain injuries has not been explored. This review discusses the mechanisms of ferroptosis and recent evidence suggesting a potential pathogenic role for ferroptosis in COVID-19-related brain injury. Furthermore, the possible routes through which SARS-CoV-2 could invade the brain are also discussed. Discoveries in these areas will open possibilities for treatment strategies to prevent or reduce brain-related complications of COVID-19.<br /><br />Among these mechanisms, ferroptosis may contribute to the pathogenesis of COVID-19-related brain injuries. First described in 2012, Dixon etal explained that ferroptosis is an iron-dependent programmed nonapoptotic cell death with unique biological processes and pathophysiologic characteristics. The pathogenic processes of ferroptosis involve an excessive iron metabolism that produces iron-dependent oxidative stress and causes damage to nucleic acids, proteins, and lipids that eventually induce cell death.Ferroptosis has recently gained considerable attention in brain research and has significant implications for several neurologic diseases, such as ischemic stroke, intracerebral hemorrhage (ICH), Alzheimer’s disease, and Parkinson’s disease. In addition, emerging evidence indicates that ferroptosis is a nexus between metabolism, redox biology, and human diseases such as COVID-19. However, the specific underlying mechanisms of ferroptosis remain unclear. Exploring the role of ferroptosis in COVID-19 infection and COVID-19-related brain injury, in particular, could be valuable for identifying therapeutic targets to prevent or lessen brain complications of COVID-19 and improve prognosis. In this regard, brain-permeable ferroptosis inhibitors or iron-chelating agents could be tested to assess whether they affect neuropsychiatric symptoms caused by COVID-19-related brain injuries.<br /><br /><br />