Glucose metabolism: A link between traumatic brain injury and Alzheimer's disease.
10.1016/j.cjtee.2020.10.001
- VernacularTitle:Glucose metabolism: A link between traumatic brain injury and Alzheimer's disease
- Author:
Xiao-Jian XU
1
;
Meng-Shi YANG
2
;
Bin ZHANG
2
;
Fei NIU
1
;
Jin-Qian DONG
2
;
Bai-Yun LIU
3
,
4
Author Information
1. Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, 100070, China.
2. Beijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
3. Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, 100070, China; Beijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China; Nerve Injury and Repair Center of Beijing Institute for Brain Disorders, Beijing, 100070, China; China National Clinical Research Center for Neurological Diseases, Beijing, 100070, China. Electronic address: liubaiyun1212@
4. com.
- Publication Type:Journal Article
- Keywords:
Alzheimer’s disease;
Glucose metabolism;
Neurological disorder;
Traumatic brain injury
- From:
Chinese Journal of Traumatology
2021;24(1):5-10
- CountryChina
- Language:English
-
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.
