@article{ref1,
title="Glucose metabolism: a link between traumatic brain injury and Alzheimer's disease",
journal="Chinese journal of traumatology",
year="2020",
author="Xu, Xiao-Jian and Yang, Meng-Shi and Zhang, Bin and Niu, Fei and Dong, Jin-Qian and Liu, Bai-Yun",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="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.<p /> <p>Language: en</p>",
language="en",
issn="1008-1275",
doi="10.1016/j.cjtee.2020.10.001",
url="http://dx.doi.org/10.1016/j.cjtee.2020.10.001"
}