Glucose metabolism: A link between traumatic brain injury and Alzheimer's disease

• 作者: Xu Xiao-Jian Yang Meng-Shi Zhang Bin Niu Fei Dong Jin-Qian Liu Bai-Yun
• 来源期刊: 中华创伤杂志英文版
• 关键词: Alzheimer's disease Traumatic brain injury Glucose metabolism Neurological disorder
• 年，卷（期）: 2021,（1）
• 所属期刊栏目: Review Article
• 页码范围: 5-10
• 页数: 6页
• 语种: 中文
• DOI: 10.1016/j.cjtee.2020.10.001

摘要

Traumatic brain injury (TBI), a growing public health problem, is a leading cause of death and disability worldwide, although its prevention measures and clinical cares are substantially improved. Increasing evidence shows that TBI may increase the risk of mood disorders and neurodegenerative diseases, including Alzheimer's disease (AD). However, the complex relationship between TBI and AD remains elusive. Metabolic dysfunction has been the common pathology in both TBI and AD. On the one hand, TBI perturbs the glucose metabolism of the brain, and causes energy crisis and subsequent hyperglycolysis. On the other hand, glucose deprivation promotes amyloidogenesis via β-site APP cleaving enzyme-1 dependent mechanism, and triggers tau pathology and synaptic function. Recent findings suggest that TBI might facilitate Alzheimer's pathogenesis by altering metabolism, which provides clues to metabolic link between TBI and AD. In this review, we will explore how TBI-induced metabolic changes contribute to the development of AD.