Endocannabinoid Metabolism and Traumatic Brain Injury.
Endocannabinoid Metabolism and Traumatic Brain Injury.
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作者：
Zhu D;Gao F;Chen C
创伤性脑损伤是致残率和致残率的主要原因，也是阿尔茨海默病等神经退行性疾病的危险因素。然而，目前还没有有效的治疗方法来治疗脑损伤引起的阿尔茨海默病。内源性大麻素是一种内源性脂质介质，参与多种生理和病理过程。化合物2-花生四烯基甘油(2-AG)是含量最丰富的内源性大麻素，具有深刻的抗炎和神经保护作用。该分子主要由单酰基甘油脂肪酶(MAGL)代谢，MAGL是降解大脑中约85%的2-AG的关键酶。使用炎症、AD和脑外伤动物模型的研究表明，MAGL的失活可以增强2-AG信号并减少其代谢产物，具有神经保护作用，表明MAGL是治疗神经退行性疾病的有前景的靶点。在这篇简短的综述中，我们综述了抑制2-AG代谢以减轻脑损伤后的神经病理以及改善突触和认知功能的研究进展。
Traumatic brain injury (TBI) represents a major cause of morbidity and disability and is a risk factor for developing neurodegenerative diseases, including Alzheimer’s disease (AD). However, no effective therapies are currently available for TBI-induced AD-like disease. Endocannabinoids are endogenous lipid mediators involved in a variety of physiological and pathological processes. The compound 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid with profound anti-inflammatory and neuroprotective properties. This molecule is predominantly metabolized by monoacylglycerol lipase (MAGL), a key enzyme degrading about 85% of 2-AG in the brain. Studies using animal models of inflammation, AD, and TBI provide evidence that inactivation of MAGL, which augments 2-AG signaling and reduces its metabolites, exerts neuroprotective effects, suggesting that MAGL is a promising therapeutic target for neurodegenerative diseases. In this short review, we provide an overview of the inhibition of 2-AG metabolism for the alleviation of neuropathology and the improvement of synaptic and cognitive functions after TBI.
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