Cruz-Haces Marcela, Tang Jonathan, Acosta Glen, Fernandez Joseph, Shi Riyi
Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907 USA.
Department of Basic Medical Sciences, Purdue University, West Lafayette, USA.
Transl Neurodegener. 2017 Jul 11;6:20. doi: 10.1186/s40035-017-0088-2. eCollection 2017.
Traumatic brain injury is among the most common causes of death and disability in youth and young adults. In addition to the acute risk of morbidity with moderate to severe injuries, traumatic brain injury is associated with a number of chronic neurological and neuropsychiatric sequelae including neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. However, despite the high incidence of traumatic brain injuries and the established clinical correlation with neurodegeneration, the causative factors linking these processes have not yet been fully elucidated. Apart from removal from activity, few, if any prophylactic treatments against post-traumatic brain injury neurodegeneration exist. Therefore, it is imperative to understand the pathophysiological mechanisms of traumatic brain injury and neurodegeneration in order to identify potential factors that initiate neurodegenerative processes. Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been implicated in both secondary brain injury and neurodegeneration. In particular, reactive oxygen species appear to be key in mediating molecular insult in neuroinflammation and excitotoxicity. As such, it is likely that post injury oxidative stress is a key mechanism which links traumatic brain injury to increased risk of neurodegeneration. Consequently, reactive oxygen species and their subsequent byproducts may serve as novel fluid markers for identification and monitoring of cellular damage. Furthermore, these reactive species may further serve as a suitable therapeutic target to reduce the risk of post-injury neurodegeneration and provide long term quality of life improvements for those suffering from traumatic brain injury.
创伤性脑损伤是青年人和年轻成年人死亡和残疾的最常见原因之一。除了中重度损伤带来的急性发病风险外，创伤性脑损伤还与许多慢性神经和神经精神后遗症相关，包括神经退行性疾病，如阿尔茨海默病和帕金森病。然而，尽管创伤性脑损伤的发病率很高，且与神经退行性变已确立临床关联，但连接这些过程的致病因素尚未完全阐明。除了停止活动外，几乎没有针对创伤性脑损伤后神经退行性变的预防性治疗方法。因此，了解创伤性脑损伤和神经退行性变的病理生理机制，以确定启动神经退行性变过程的潜在因素至关重要。氧化应激、神经炎症和谷氨酸能兴奋性毒性先前已被认为与继发性脑损伤和神经退行性变有关。特别是，活性氧似乎是介导神经炎症和兴奋性毒性中分子损伤的关键因素。因此，损伤后的氧化应激很可能是将创伤性脑损伤与神经退行性变风险增加联系起来的关键机制。因此，活性氧及其随后的副产物可能作为识别和监测细胞损伤的新型液体标志物。此外，这些活性物质可能进一步作为合适的治疗靶点，以降低损伤后神经退行性变的风险，并为创伤性脑损伤患者提供长期生活质量改善。
