降钙素基因相关肽及其在治疗创伤性脑损伤、蛛网膜下腔出血和相关偏头痛中的临床应用

Y. Mehkri, Maxwell G. Woolridge, B. Lucke-Wold
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引用次数: 0

摘要

降钙素基因相关肽(CGRP)是一种强效的血管舒张剂和神经递质,在偏头痛的病理生理学背景下得到了广泛的研究。最近,研究探索了它在治疗创伤性脑损伤(TBI)和蛛网膜下腔出血(SAH)中的作用。尽管偏头痛有多种治疗方法,但对神经损伤后偏头痛的治疗研究很少。随着TBI的发病率持续增长,特别是在美国,有必要探索其他治疗方案,如CGRP抑制(CGRPi)。考虑到CGRPi在TBI和SAH中的不同作用,下一步重要的是观察CGRPi治疗的TBI和蛛网膜下腔出血患者与单独TBI患者的反应如何不同。还有必要对严重TBI患者进行研究,这些患者可以从这种新策略中获益最多。降钙素基因相关肽(CGRP)是一种37个氨基酸的神经递质,已被证明与颅骨和面部病理有关。最常见的是,CGRP作为一种强效血管舒张剂的作用[1,2]与偏头痛有关[3]。最近,文献中对其在治疗创伤性脑损伤[3-5]和蛛网膜下腔出血(SAH)[6-9]中的应用进行了探讨。尽管对小鼠和其他动物模型进行了大量研究,描述了外源性CGRP的治疗效果,但由于其半衰期低,其在人类中的疗效有限[10],阻碍了其进入人体试验。偏头痛
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Commentary: Calcitonin Gene Related Peptide and Its Clinical Utility for the Treatment of Traumatic Brain Injury, Subarachnoid Hemorrhage and Associated Migraine
Commentary Calcitonin gene related peptide (CGRP) is a potent vasodilator and neurotransmitter that has been extensively studied in the context of migraine pathophysiology. Recently, studies have explored its role in the treatment of traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH). Although a multitude of therapies exist for migraine, there has been little study on the management of migraine following neurologic injury. As the incidence of TBI continues to grow, especially in the United States, it is essential to explore additional therapeutic options such as CGRP inhibition (CGRPi). Given its differential effects in TBI and SAH, an important next step is to see how patients with both TBI and SAH treated with CGRPi respond differently than patients with TBI alone. There is also a need for study in patients with severe TBI who could benefit most from this novel strategy. Calcitonin gene-related peptide (CGRP) is a 37-amino acid neurotransmitter that has been shown to be involved in cranial and facial pathology. Most commonly, CGRP’s role as a potent vasodilator [1,2] has been associated with migraine [3]. It’s use in the treatment of traumatic brain injury [3–5] and subarachnoid hemorrhage (SAH) [6–9] has recently been explored in the literature. While there have been numerous studies on mice and other animal models describing exogenous CGRP’s therapeutic effects, its limited efficacy in humans due to its low half-life [10] has prevented its advancement to human trials. Migraines
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