According to the World Health Organization, perinatal asphyxia is the leading cause of severe neurological disabilities and the second leading cause of neonatal death among term infants, with an incidence of 3.94-5.12 per 1,000 live births. Perinatal asphyxia leads to neonatal hypoxic-ischemic encephalopathy, which remains a common cause of neonatal death and long-term disabilities, affecting 1.5-3 per 1,000 live births in developed countries and up to 26 per 1,000 live births in developing countries. This condition is characterized by altered levels of consciousness or manifests with seizures, often associated with difficulties in initiating and maintaining breathing, as well as depression of tone and reflexes. Currently, therapeutic hypothermia is the standard treatment for neonates with moderate to severe hypoxic-ischemic encephalopathy; however, it does not provide complete neuroprotection and is only partially effective. Therefore, new treatments with good therapeutic windows are urgently needed to ensure the best possible preservation of neurological tissue for patients exposed to hypoxic-ischemic insult. Traumatic brain injury is a common cause of morbidity and mortality among children and young adults in developed countries. The incidence of traumatic brain injury has increased in recent years, yet the prognosis for these patients has not substantially changed. In recent studies the key intermediary role of the immune system and neuroinflammation has been proposed to explain the pathophysiology of traumatic brain injury, both in the acute phase and in the long term. Indeed, neuroinflammatory processes can persist for several months, contributing to chronic alterations and accelerating brain aging in patients with post-traumatic brain injury. Currently, therapies that have shown promising results in patients with post-traumatic brain injuries are unfortunately still limited, especially in the context of severe traumatic brain injury. Thus, there is an urgent need for new treatments with a broader therapeutic window that can counteract early and chronic pathophysiological events.