Neurological disorders are associated with increased oxidative stress. Reactive oxidants damage tissue and promote cell death, but it is apparent that oxidants can have more subtle effects on cell function through the modulation of redox-sensitive signalling pathways. Cells of the blood-brain barrier regulate the brain microenvironment but become dysfunctional during neurological disease. The blood-brain barrier is maintained by many cell types, and is modulated by redox-sensitive pathways, ranging from the cytoskeletal elements responsible for establishing a barrier, to growth factor and cytokine signalling pathways that influence neurovascular cells. During neurological disease, blood-brain barrier cells are exposed to exogenously generated oxidants from immune cells, as well as increasing endogenously oxidant production. These oxidants impair the function of the blood-brain barrier, leading to increased leakage and reduced blood flow. Reducing the impact of oxidants on the function of blood-brain barrier cells may provide new strategies for delaying the progression of neurological disease.

神经系统疾病与氧化应激增加有关。活性氧化剂会损害组织并促进细胞死亡，但是很明显，氧化剂可以通过调节氧化还原敏感的信号通路对细胞功能产生更细微的影响。血脑屏障细胞调节大脑的微环境，但在神经系统疾病中功能失调。血脑屏障由许多细胞类型维持，并受氧化还原敏感途径的调节，这些途径从负责建立屏障的细胞骨架元件到影响神经血管细胞的生长因子和细胞因子信号传导途径。在神经系统疾病期间，血脑屏障细胞会暴露于免疫细胞产生的外源性氧化剂，并会增加内源性氧化剂的产生。这些氧化剂削弱了血脑屏障的功能，导致泄漏增加和血流减少。减少氧化剂对血脑屏障细胞功能的影响可能为延迟神经系统疾病的进展提供新的策略。