Djordjevic Jelena, Sabbir Mohammad Golam, Albensi Benedict C
Division of Neurodegenerative Disorders, St. Boniface Hospital Research Winnipeg, Manitoba, Canada.
Curr Alzheimer Res. 2016;13(7):730-8. doi: 10.2174/1567205013666160222110320.
Traumatic brain injury (TBI) has become a significant medical and social concern within the last 30 years. TBI has acute devastating effects, and in many cases, seems to initiate long-term neurodegeneration. With advances in medical technology, many people are now surviving severe brain injuries and their long term consequences. Post trauma effects include communication problems, sensory deficits, emotional and behavioral problems, physical complications and pain, increased suicide risk, dementia, and an increased risk for chronic CNS diseases, such as Alzheimer's disease (AD). In this review, we provide an introduction to TBI and hypothesize how it may lead to neurodegenerative disease in general and AD in particular. In addition, we discuss the evidence that supports the hypothesis that TBI may lead to AD. In particular, we focus on inflammatory responses as key processes in TBI-induced secondary injury, with emphasis on nuclear factor kappa B (NF-κB) signaling.
在过去30年里,创伤性脑损伤(TBI)已成为一个重大的医学和社会问题。TBI具有急性破坏性影响,而且在许多情况下,似乎会引发长期神经退行性变。随着医学技术的进步,现在许多严重脑损伤患者得以存活并承受其长期后果。创伤后影响包括沟通问题、感觉缺陷、情绪和行为问题、身体并发症和疼痛、自杀风险增加、痴呆以及慢性中枢神经系统疾病(如阿尔茨海默病(AD))风险增加。在本综述中,我们对TBI进行了介绍,并推测它一般如何导致神经退行性疾病,特别是AD。此外,我们讨论了支持TBI可能导致AD这一假说的证据。特别是,我们将重点放在炎症反应作为TBI诱导继发性损伤的关键过程,尤其关注核因子κB(NF-κB)信号传导。