Mood and Anxiety Program, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA.
Veterans Health Administration, Rocky Mountain Mental Illness Research Education and Clinical Center (MIRECC), Veterans Integrated Service Network (VISN) 19, Aurora, CO, USA.
J Alzheimers Dis. 2020;74(1):1-28. doi: 10.3233/JAD-191150.
There is an increasing evidence that inflammation contributes to clinical and functional outcomes in traumatic brain injury (TBI). Many successful target-engaging, lesion-reducing, symptom-alleviating, and function-improving interventions in animal models of TBI have failed to show efficacy in clinical trials. Timing and immunological context are paramount for the direction, quality, and intensity of immune responses to TBI and the resulting neuroanatomical, clinical, and functional course. We present components of the immune system implicated in TBI, potential immune targets, and target-engaging interventions. The main objective of our article is to point toward modifiable molecular and cellular mechanisms that may modify the outcomes in TBI, and contribute to increasing the translational value of interventions that have been identified in animal models of TBI.
越来越多的证据表明,炎症会导致创伤性脑损伤(TBI)的临床和功能结果恶化。许多在 TBI 动物模型中成功的靶向干预、减少损伤、缓解症状和改善功能的干预措施,在临床试验中都未能显示出疗效。在 TBI 中,时间和免疫学背景对于免疫反应的方向、质量和强度以及由此产生的神经解剖学、临床和功能过程至关重要。我们提出了与 TBI 相关的免疫系统成分、潜在的免疫靶点和靶向干预措施。本文的主要目的是指出可能改变 TBI 结果的可调节的分子和细胞机制,并有助于提高已在 TBI 动物模型中确定的干预措施的转化价值。