Bourgeois-Tardif Sandrine, De Beaumont Louis, Rivera José Carlos, Chemtob Sylvain, Weil Alexander G
Department of Neuroscience, University of Montreal, Montreal, Canada.
Hopital du Sacre-Coeur de Montreal, Universite de Montreal - Psychology, Montreal, QC, Canada.
Neurol Sci. 2021 Apr;42(4):1287-1299. doi: 10.1007/s10072-020-05002-3. Epub 2021 Jan 19.
Traumatic brain injury is one of the leading causes of morbidity and mortality throughout the world. Its increasing incidence, in addition to its fundamental role in the development of neurodegenerative disease, proves especially concerning. Despite extensive preclinical and clinical studies, researchers have yet to identify a safe and effective neuroprotective strategy. Following brain trauma, secondary injury from molecular, metabolic, and cellular changes causes progressive cerebral tissue damage. Chronic neuroinflammation following traumatic brain injuries is a key player in the development of secondary injury. Targeting this phenomenon for development of effective neuroprotective therapies holds promise. This strategy warrants a concrete understanding of complex neuroinflammatory mechanisms. In this review, we discuss pathophysiological mechanisms such as the innate immune response, glial activation, blood-brain barrier disruption, activation of immune mediators, as well as biological markers of traumatic brain injury. We then review existing and emerging pharmacological therapies that target neuroinflammation to improve functional outcome.
创伤性脑损伤是全球发病和死亡的主要原因之一。其发病率不断上升，加之在神经退行性疾病发展过程中的基础性作用，尤其令人担忧。尽管进行了广泛的临床前和临床研究，但研究人员尚未确定一种安全有效的神经保护策略。脑外伤后，分子、代谢和细胞变化引起的继发性损伤会导致脑组织进行性损伤。创伤性脑损伤后的慢性神经炎症是继发性损伤发展的关键因素。针对这一现象开发有效的神经保护疗法具有前景。该策略需要对复杂的神经炎症机制有具体的了解。在本综述中，我们讨论了诸如先天免疫反应、胶质细胞激活、血脑屏障破坏、免疫介质激活以及创伤性脑损伤的生物标志物等病理生理机制。然后，我们综述了现有的和新出现的针对神经炎症以改善功能结局的药物疗法。
