Dysregulated Glucose Metabolism as a Therapeutic Target to Reduce Post-traumatic Epilepsy.
Dysregulated Glucose Metabolism as a Therapeutic Target to Reduce Post-traumatic Epilepsy.
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DOI：
10.3389/fncel.2018.00350
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发表时间：
2018
影响因子：
5.3
通讯作者：
Dulla CG
中科院分区：
文献类型：
--
作者：
Koenig JB;Dulla CG
创伤性脑损伤 (TBI) 是全世界残疾的一个重要原因，并可能导致创伤后癫痫。损伤后会发生多种分子、细胞和网络病理，可能导致癫痫发生。确定疾病进展机制和预测临床结果的生物标志物的努力主要集中在代谢变化上。成像方法的进步与成熟的生化方法相结合，揭示了 TBI 后急剧发生的复杂代谢变化，然后在几天到几周内演变。基于这些丰富的临床和临床前数据，再加上生酮饮食等代谢疗法在治疗癫痫方面的成功，人们越来越关注确定 TBI 后控制代谢活动是否具有预防创伤后癫痫发生的治疗价值。在这里，我们重点关注创伤性脑损伤后和癫痫发作期间大脑中葡萄糖利用和糖酵解活动的变化。我们回顾了相关文献，并概述了利用糖酵解抑制剂作为创伤后癫痫疾病缓解疗法的潜在途径。
Traumatic brain injury (TBI) is a significant cause of disability worldwide and can lead to post-traumatic epilepsy. Multiple molecular, cellular, and network pathologies occur following injury which may contribute to epileptogenesis. Efforts to identify mechanisms of disease progression and biomarkers which predict clinical outcomes have focused heavily on metabolic changes. Advances in imaging approaches, combined with well-established biochemical methodologies, have revealed a complex landscape of metabolic changes that occur acutely after TBI and then evolve in the days to weeks after. Based on this rich clinical and preclinical data, combined with the success of metabolic therapies like the ketogenic diet in treating epilepsy, interest has grown in determining whether manipulating metabolic activity following TBI may have therapeutic value to prevent post-traumatic epileptogenesis. Here, we focus on changes in glucose utilization and glycolytic activity in the brain following TBI and during seizures. We review relevant literature and outline potential paths forward to utilize glycolytic inhibitors as a disease-modifying therapy for post-traumatic epilepsy.
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影响因子：
16.2
作者：
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发表时间：
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