IL1B and Sepsis: The occurrence of SAE is intricately linked to various factors, including the release of inflammatory mediators, dysregulation of cerebral vascular autoregulation, impairment of blood-brain barrier function, and neuronal apoptosis.[90] During sepsis, the body generates a significant amount of inflammatory mediators, such as TNF-α,[91] IL-1β,[92] and in IL-6,[93] which can directly penetrate the blood-brain barrier, thereby affecting brain tissue and causing abnormal brain function.