Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Jacksonville, FL 32224, USA.
New York Medical College, Valhalla, NY 10595, USA.
Cells. 2024 Jul 21;13(14):1228. doi: 10.3390/cells13141228.
Epilepsy is associated with substantial neuropsychiatric impairments that persist long after the onset of the condition, significantly impacting quality of life. The goal of this review was to uncover how the pathological consequences of epilepsy, such as excessive glutamate release and a disrupted blood-brain barrier (BBB), contribute to the emergence of neuropsychiatric disorders. We hypothesize that epilepsy induces a dysfunctional BBB through hyperexcitation, which then further amplifies post-ictal glutamate levels and, thus, triggers neurodegenerative and neuropsychiatric processes. This review identifies the determinants of glutamate concentration levels in the brain and explores potential therapeutic interventions that restore BBB integrity. Our focus on therapeutic BBB restoration is guided by the premise that it may improve glutamate regulation, consequently mitigating the neurotoxicity that contributes to the onset of neuropsychiatric symptoms.
癫痫与严重的神经精神损伤有关，这些损伤在疾病发作后持续存在，严重影响生活质量。本综述的目的是揭示癫痫的病理后果，如过度释放谷氨酸和血脑屏障（BBB）破坏，如何导致神经精神障碍的出现。我们假设癫痫通过过度兴奋导致 BBB 功能障碍，进而进一步放大癫痫发作后的谷氨酸水平，从而触发神经退行性和神经精神过程。本综述确定了大脑中谷氨酸浓度水平的决定因素，并探讨了恢复 BBB 完整性的潜在治疗干预措施。我们关注治疗性 BBB 修复，是基于这样一个前提，即它可能改善谷氨酸调节，从而减轻导致神经精神症状出现的神经毒性。
