摘要
在过去的30年中创伤性脑损伤(TBI)已经成为一个重要的医学和社会问题。TBI有急性破坏性的影响,在许多情况下,似乎引起长期的神经退行性疾病。随着医疗技术的进步,现在很多人都存活于严重的脑损伤及伴随长期的后遗症。创伤后的影响包括沟通问题,感觉障碍,情绪和行为问题,身体的并发症和疼痛,增加了自杀、痴呆症、和慢性中枢神经系统疾病如阿尔茨海默氏病(AD)的风险。在这篇综述中,我们介绍了创伤性脑损伤TBI和假设它大致上可能导致神经退行性疾病,尤其是阿尔茨海默氏病(AD)。此外,我们讨论了支持创伤性脑损伤(TBI)可能导致阿尔茨海默氏病(AD)这一假设的证据,我们专注于在脑外伤引起的继发性损伤里炎症反应是关键的过程,强调了核因子-κB (NF-κB)的信号转导。
关键词: 阿尔茨海默病,炎症,线粒体,核因子-κB,创伤性脑损伤。
Current Alzheimer Research
Title:Traumatic Brain Injury as a Risk Factor for Alzheimer’s Disease: Is Inflammatory Signaling a Key Player?
Volume: 13 Issue: 7
Author(s): Jelena Djordjevic, Mohammad Golam Sabbir, Benedict C. Albensi
Affiliation:
关键词: 阿尔茨海默病,炎症,线粒体,核因子-κB,创伤性脑损伤。
摘要: 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.
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Cite this article as:
Jelena Djordjevic, Mohammad Golam Sabbir, Benedict C. Albensi , Traumatic Brain Injury as a Risk Factor for Alzheimer’s Disease: Is Inflammatory Signaling a Key Player?, Current Alzheimer Research 2016; 13 (7) . https://dx.doi.org/10.2174/1567205013666160222110320
DOI https://dx.doi.org/10.2174/1567205013666160222110320 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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