Gupta Rajaneesh, Sen Nilkantha
Rev Neurosci. 2016 Jan;27(1):93-100. doi: 10.1515/revneuro-2015-0017.
Traumatic brain injury (TBI), a major global health and socioeconomic problem, is now established as a chronic disease process with a broad spectrum of pathophysiological symptoms followed by long-term disabilities. It triggers multiple and multidirectional biochemical events that lead to neurodegeneration and cognitive impairment. Recent studies have presented strong evidence that patients with TBI history have a tendency to develop proteinopathy, which is the pathophysiological feature of neurodegenerative disorders such as Alzheimer disease (AD), chronic traumatic encephalopathy (CTE), and amyotrophic lateral sclerosis (ALS). This review mainly focuses on mechanisms related to AD, CTE, and ALS that are induced after TBI and their relevance to the advancement of these neurodegenerative diseases. This review encompasses acute effects and chronic neurodegenerative consequences after TBI for a better understanding of TBI-induced neuronal death and to design therapies that will effectively treat patients in the primary or secondary progressive stages.
创伤性脑损伤(TBI)是一个重大的全球健康和社会经济问题,目前已被确认为一种慢性疾病过程,伴有广泛的病理生理症状,并导致长期残疾。它引发多种多向性生化事件,导致神经退行性变和认知障碍。最近的研究提供了强有力的证据,表明有TBI病史的患者倾向于发生蛋白病,这是阿尔茨海默病(AD)、慢性创伤性脑病(CTE)和肌萎缩侧索硬化症(ALS)等神经退行性疾病的病理生理特征。本综述主要关注TBI后诱发的与AD、CTE和ALS相关的机制,以及它们与这些神经退行性疾病进展的相关性。本综述涵盖了TBI后的急性效应和慢性神经退行性后果,以便更好地理解TBI诱导的神经元死亡,并设计出能够有效治疗原发性或继发性进展阶段患者的疗法。