Castellani Rudy J
Division of Neuropathology, University of Maryland School of Medicine, Baltimore, MD, USA.
Lab Invest. 2015 Jun;95(6):576-84. doi: 10.1038/labinvest.2015.54. Epub 2015 Apr 13.
Chronic traumatic encephalopathy (CTE) has been in the medical literature since the 1920s. It is characterized clinically by diverse neuropsychiatric symptoms, and pathologically by variable degrees of phosphorylated tau accumulation in the brain. The evolving paradigm for the pathogenesis of CTE suggests that concussion or subconcussion from athletic participation initiates a cascade of pathologic events, encompassing neuroinflammation and protein templating with trans-synaptic neurotoxicity. The end result is neurologic and neurobehavioral deterioration, often with self-harm. Although these concepts warrant further investigation, the available evidence permits no conclusions as regards the pathogenesis of the reported findings. Investigations into the role of premorbid or co-morbid neurodegenerative diseases has been limited to date, and in-depth genetic analyses have not been performed. The role of concussion or subconcussion if any, whether and how the condition progresses over time, the extent of phosphorylated tau in clinically normal athletes, the role of phosphorylated tau as a toxic species versus an inert disease response, and whether protein templating has any in vivo relevance remain to be elucidated.
自20世纪20年代以来，慢性创伤性脑病（CTE）就已出现在医学文献中。其临床特征为多种神经精神症状，病理特征为大脑中不同程度的磷酸化tau蛋白积累。CTE发病机制的不断演变的模式表明，运动参与导致的脑震荡或轻微脑震荡引发了一系列病理事件，包括神经炎症和具有跨突触神经毒性的蛋白质模板化。最终结果是神经和神经行为恶化，常伴有自我伤害。尽管这些概念值得进一步研究，但现有证据无法就所报告发现的发病机制得出结论。迄今为止，对病前或共病神经退行性疾病作用的研究有限，尚未进行深入的基因分析。脑震荡或轻微脑震荡（若有）的作用、病情是否以及如何随时间进展、临床正常运动员中磷酸化tau蛋白的程度、磷酸化tau蛋白作为有毒物质与惰性疾病反应的作用，以及蛋白质模板化是否具有任何体内相关性仍有待阐明。
