Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research (STAR), National Study Center for Trauma and EMS, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Int J Mol Sci. 2014 Jan 17;15(1):1216-36. doi: 10.3390/ijms15011216.
Traumatic brain injury (TBI) induces secondary biochemical changes that contribute to delayed neuroinflammation, neuronal cell death, and neurological dysfunction. Attenuating such secondary injury has provided the conceptual basis for neuroprotective treatments. Despite strong experimental data, more than 30 clinical trials of neuroprotection in TBI patients have failed. In part, these failures likely reflect methodological differences between the clinical and animal studies, as well as inadequate pre-clinical evaluation and/or trial design problems. However, recent changes in experimental approach and advances in clinical trial methodology have raised the potential for successful clinical translation. Here we critically analyze the current limitations and translational opportunities for developing successful neuroprotective therapies for TBI.
创伤性脑损伤（TBI）引起的继发性生化变化导致延迟性神经炎症、神经元细胞死亡和神经功能障碍。减轻这种继发性损伤为神经保护治疗提供了概念基础。尽管有强有力的实验数据，但超过 30 项 TBI 患者的神经保护临床试验都失败了。部分原因可能是临床和动物研究之间的方法学差异，以及临床前评估不足和/或试验设计问题。然而，最近实验方法的改变和临床试验方法学的进步提高了成功转化为临床应用的潜力。在这里，我们批判性地分析了开发 TBI 成功神经保护疗法的当前局限性和转化机会。
