Vile Alexander R, Atkinson Leigh
James Cook University College of Medicine and Dentistry, Australia.
Wesley Pain and Spine Centre, Brisbane, QLD, Australia.
J Clin Neurosci. 2017 Jul;41:24-29. doi: 10.1016/j.jocn.2017.03.035. Epub 2017 Mar 27.
This review aims to integrate current literature on the pathogenic mechanisms of Chronic Traumatic Encephalopathy (CTE) to create a multifactorial understanding of the disease. CTE is a progressive neurodegenerative disease, classed as a tauopathy, although it appears the pathogenic mechanisms are more complex than this. It affects those with a history of repetitive mild traumatic brain injury. Currently, there are no treatments for CTE and the disease can only be affirmatively diagnosed in post mortem. Understanding the pathogenesis of the disease will provide an avenue to explore possible treatment and diagnostic modalities. The pathological hallmarks of CTE have been well characterised and have been linked to the pathophysiologic mechanisms in this review. Human studies are limited due to ethical implications of exposing subjects to head trauma. Phosphorylation of tau, microglial activation, TAR DNA-binding protein 43 and diffuse axonal injury have all been implicated in the pathogenesis of CTE. The neuronal loss and axonal dysfunction mediated by these pathognomonic mechanisms lead to the broad psycho-cognitive symptoms seen in CTE.
本综述旨在整合当前关于慢性创伤性脑病（CTE）致病机制的文献，以对该疾病形成多因素的理解。CTE是一种进行性神经退行性疾病，归类为tau蛋白病，尽管其致病机制似乎比这更为复杂。它影响有重复性轻度创伤性脑损伤病史的人群。目前，尚无针对CTE的治疗方法，且该疾病只能在尸检时得到肯定诊断。了解该疾病的发病机制将为探索可能的治疗和诊断方式提供途径。CTE的病理特征已得到充分表征，并在本综述中与病理生理机制相关联。由于让受试者暴露于头部创伤存在伦理问题，人体研究受到限制。tau蛋白磷酸化、小胶质细胞激活、TAR DNA结合蛋白43和弥漫性轴索损伤均与CTE的发病机制有关。由这些特征性机制介导的神经元丢失和轴索功能障碍导致了CTE中出现的广泛心理认知症状。
