Al-Rubaie Ali
Department of Biomedical, Health and Exercise Sciences, School of Health Sciences, Swinburne University of Technology, Hawthorn, Victoria, Australia.
J Clin Neurol. 2025 Jul;21(4):265-276. doi: 10.3988/jcn.2025.0079.
Traumatic brain injury (TBI) is one of the main mechanisms underlying health issues associated with functional and structural brain changes. While direct effects such as cognitive and physical impairments are well documented, recent research has linked TBI to neurodegenerative changes similar to dementia. TBI-related neurodegeneration includes progressive brain-tissue degeneration that leads to behavioral changes, cognitive decline, and dementia-like symptoms. The exact underlying mechanisms are complex, and include neuroinflammation, oxidative stress, excitotoxicity, and disruption to protein homeostasis. Neuroinflammation is controlled by the activation of astrocytes and microglia and causes neuronal damage and the prolonged release of proinflammatory cytokines. Oxidative stress damages cell and impairs mitochondrial function, while the accumulation of misfolded proteins such as tau and β-amyloid mimics the pathology of Alzheimer's disease. Excitotoxicity involves excessive neurotransmitter release that may lead to further injuries. Epidemiological studies show that the risk of dementia is increased after moderate-to-severe TBI and influenced by age and genetic factors. Current management strategies focus on symptom relief, and there is ongoing research aimed at improving the understanding of the underlying mechanisms and the development of effective treatments.
创伤性脑损伤(TBI)是与大脑功能和结构变化相关的健康问题的主要潜在机制之一。虽然认知和身体损伤等直接影响已有充分记录,但最近的研究已将TBI与类似于痴呆症的神经退行性变化联系起来。与TBI相关的神经退行性变包括导致行为改变、认知衰退和痴呆样症状的进行性脑组织退化。确切的潜在机制很复杂,包括神经炎症、氧化应激、兴奋性毒性以及蛋白质稳态的破坏。神经炎症由星形胶质细胞和小胶质细胞的激活控制,并导致神经元损伤和促炎细胞因子的长期释放。氧化应激会损害细胞并削弱线粒体功能,而错误折叠蛋白(如tau蛋白和β-淀粉样蛋白)的积累则模拟了阿尔茨海默病的病理过程。兴奋性毒性涉及神经递质的过度释放,这可能导致进一步的损伤。流行病学研究表明,中重度TBI后患痴呆症的风险会增加,且受年龄和遗传因素影响。目前的管理策略侧重于缓解症状,并且正在进行研究,旨在增进对潜在机制的理解并开发有效的治疗方法。