Yang W-J, Chen W, Chen L, Guo Y-J, Zeng J-S, Li G-Y, Tong W-S
Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
Acta Neurol Scand. 2017 Jun;135(6):622-627. doi: 10.1111/ane.12644. Epub 2016 Jul 21.
Traumatic brain injury (TBI) results in significant morbidity and mortality throughout the world. In TBI patients suffering cognitive, emotional, and behavioral deficits, the leading cause derives from the physical injury to the central nervous system (CNS) that impairs brain function.
Here, we applied a targeted approach to understand the potential mechanisms of neuron damage after TBI. Tau protein phosphorylation was compared in the brain tissues collected from patients underwent brain surgery based on the assessment of brain injury extent by Glasgow Coma Scale (GCS).
The results indicated that the levels of phosphorylated tau were significantly higher in the severe and extremely severe TBI groups, compared to the moderate group of patients. Phosphorylated, but not the total tau protein was uniquely correlated with the GCS score (R =.7849, P<.01) in 142 TBI patients. Consistently, the activities of key players associated with tau hyperphosphorylation GSK-3β and PP2A showed parallel correlations with the severity of TBI as well.
These data suggest that the enhanced tau protein phosphorylation occurs upon severe neuron injures and may contribute to the pathological structural changes of CNS leading to brain damage of TBI.
创伤性脑损伤（TBI）在全球范围内导致了显著的发病率和死亡率。在患有认知、情感和行为缺陷的TBI患者中，主要原因源于中枢神经系统（CNS）的物理损伤，这种损伤会损害脑功能。
在此，我们采用了一种靶向方法来了解TBI后神经元损伤的潜在机制。基于格拉斯哥昏迷量表（GCS）对脑损伤程度的评估，比较了接受脑部手术患者脑组织中的tau蛋白磷酸化情况。
结果表明，与中度TBI患者组相比，重度和极重度TBI组中磷酸化tau的水平显著更高。在142例TBI患者中，磷酸化而非总tau蛋白与GCS评分唯一相关（R = 0.7849，P < 0.01）。同样，与tau过度磷酸化相关的关键因子GSK-3β和PP2A的活性也与TBI的严重程度呈平行相关。
这些数据表明，在严重神经元损伤时tau蛋白磷酸化增强，可能导致CNS的病理结构变化，进而导致TBI脑损伤。
