Clinical Neurochemistry Laboratory, Institue of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, SE-431 80 Mölndal, Sweden.
Neuron. 2012 Dec 6;76(5):886-99. doi: 10.1016/j.neuron.2012.11.021.
The acute and long-term consequences of traumatic brain injury (TBI) have received increased attention in recent years. In this Review, we discuss the neuropathology and neural mechanisms associated with TBI, drawing on findings from sports-induced TBI in athletes, in whom acute TBI damages axons and elicits both regenerative and degenerative tissue responses in the brain and in whom repeated concussions may initiate a long-term neurodegenerative process called dementia pugilistica or chronic traumatic encephalopathy (CTE). We also consider how the neuropathology and neurobiology of CTE in many ways resembles other neurodegenerative illnesses such as Alzheimer's disease, particularly with respect to mismetabolism and aggregation of tau, β-amyloid, and TDP-43. Finally, we explore how translational research in animal models of acceleration/deceleration types of injury relevant for concussion together with clinical studies employing imaging and biochemical markers may further elucidate the neurobiology of TBI and CTE.
近年来，创伤性脑损伤（TBI）的急性和长期后果受到了越来越多的关注。在这篇综述中，我们讨论了与 TBI 相关的神经病理学和神经机制，借鉴了运动员运动引起的 TBI 的发现，在运动员中，急性 TBI 损伤轴突，并在大脑中引发再生和退行性组织反应，而反复脑震荡可能引发一种称为拳击手痴呆或慢性创伤性脑病（CTE）的长期神经退行性过程。我们还考虑了 CTE 的神经病理学和神经生物学在许多方面如何类似于其他神经退行性疾病，如阿尔茨海默病，特别是在代谢紊乱和 tau、β-淀粉样蛋白和 TDP-43 的聚集方面。最后，我们探讨了与脑震荡相关的加速/减速类型损伤的动物模型中的转化研究以及使用影像学和生化标志物的临床研究如何进一步阐明 TBI 和 CTE 的神经生物学。
