Department of Clinical and Experimental Medicine, University of Messina, Piazza Pugliatti 1, 98122 Messina, Italy.
IRCCS Centro Neurolesi Bonino-Pulejo, S.S. 113 Via Palermo, C.da Casazza, 98124 Messina, Italy.
Int J Mol Sci. 2024 Oct 31;25(21):11708. doi: 10.3390/ijms252111708.
Neuroplasticity and neuroinflammation are variables seen during recovery from traumatic brain injury (TBI), while biomarkers are useful in monitoring injury and guiding rehabilitation efforts. This systematic review examines how neuroinflammation affects neuroplasticity and recovery following TBI in animal models and humans. Studies were identified from an online search of the PubMed, Web of Science, and Embase databases without any search time range. This review has been registered on Open OSF (n) UDWQM. Recent studies highlight the critical role of biomarkers like serum amyloid A1 (SAA1) and Toll-like receptor 4 (TLR4) in predicting TBI patients' injury severity and recovery outcomes, offering the potential for personalized treatment and improved neurorehabilitation strategies. Additionally, insights from animal studies reveal how neuroinflammation affects recovery, emphasizing targets such as NOD-like receptor family pyrin domain-containing 3 (NLRP3) and microglia for enhancing therapeutic interventions. This review emphasizes the central role of neuroinflammation in TBI, and its adverse impact on neuroplasticity and recovery, and suggests that targeted anti-inflammatory treatments and biomarker-based personalized approaches hold the key to improvement. Such approaches will need further development in future research by integrating neuromodulation and pharmacological interventions, along with biomarker validation, to optimize management in TBI.
神经可塑性和神经炎症是创伤性脑损伤 (TBI) 恢复过程中观察到的变量，而生物标志物在监测损伤和指导康复努力方面很有用。本系统评价检查了神经炎症如何影响动物模型和人类 TBI 后的神经可塑性和恢复。研究是通过在线搜索 PubMed、Web of Science 和 Embase 数据库而确定的，没有任何搜索时间范围。本综述已在 Open OSF（n）UDWQM 上注册。最近的研究强调了生物标志物（如血清淀粉样蛋白 A1 (SAA1) 和 Toll 样受体 4 (TLR4)）在预测 TBI 患者损伤严重程度和恢复结果方面的关键作用，为个性化治疗和改进神经康复策略提供了可能。此外，动物研究的见解揭示了神经炎症如何影响恢复，强调了 NOD 样受体家族吡喃结构域包含 3 (NLRP3) 和小胶质细胞等靶点，以增强治疗干预。本综述强调了神经炎症在 TBI 中的核心作用及其对神经可塑性和恢复的不利影响，并表明靶向抗炎治疗和基于生物标志物的个性化方法是改善的关键。在未来的研究中，需要通过整合神经调节和药物干预以及生物标志物验证来进一步发展这些方法，以优化 TBI 的管理。
