Kaniuk Julia K, Kumar Divy, Mazurek Christopher, Khavari Sepehr, Sollenberger Christopher, Ahuja Arun, Mossner James M, Ahuja Christopher S
Feinberg School of Medicine, Northwestern University, 240 E Huron Street, Suite 1-200, Chicago, IL 60611, USA.
Department of Neurosurgery, The University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA 19104, USA.
Int J Mol Sci. 2025 Jul 25;26(15):7191. doi: 10.3390/ijms26157191.
Traumatic brain injury (TBI) initiates a complex cascade of pathophysiological events that have far-reaching consequences beyond the initial injury. This review examines the current state of the literature on the mechanisms underlying neurotrauma and neuroinflammation, with particular emphasis on the molecular cross-talk between these disparate pathways that ultimately precipitates the development of chronic traumatic encephalopathy (CTE). We integrate this mechanistic knowledge with potential diagnostic biomarkers, such as glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1), and advances in neuroimaging and machine learning-based predictive tools. Finally, we discuss the current therapeutic approaches under investigation, and highlight which molecular targets have yet to be explored for potential therapeutic development.
创伤性脑损伤（TBI）引发了一系列复杂的病理生理事件，这些事件的影响远远超出了最初的损伤。本综述探讨了有关神经创伤和神经炎症潜在机制的文献现状，特别强调了这些不同途径之间的分子相互作用，这些相互作用最终促使慢性创伤性脑病（CTE）的发展。我们将这一机制知识与潜在的诊断生物标志物，如胶质纤维酸性蛋白（GFAP）、神经丝轻链（NfL）和泛素羧基末端水解酶L1（UCH-L1），以及神经影像学和基于机器学习的预测工具的进展相结合。最后，我们讨论了目前正在研究的治疗方法，并强调了哪些分子靶点尚未被探索用于潜在的治疗开发。
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