To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis.
We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance.
TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective.
Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson\'s disease, depression, and cognitive impairment.
It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.
目的:为基于调节谷氨酸稳态预防PTE的药物开发提供神经药理学见解。
方法:我们讨论了TBI如何影响谷氨酸稳态及其与PTE的关系。此外,总结了TBI后调节谷氨酸稳态的分子途径的研究进展,以及通过恢复谷氨酸平衡预防PTE的药理研究。
结果:TBI可以导致大脑中谷氨酸的积累,这增加了PTE的风险。靶向影响谷氨酸稳态的分子途径有助于恢复正常的谷氨酸水平并且具有神经保护作用。
结论:将谷氨酸稳态调节作为新药开发的手段,可以避免直接抑制谷氨酸受体引起的副作用,期望缓解与大脑中谷氨酸水平异常有关的疾病,比如PTE,帕金森病,抑郁症,和认知障碍。
结论:TBI后通过药理学方法调节谷氨酸稳态是一种有前途的策略,从而减少神经损伤和预防PTE。