Activation of brain glucose metabolism ameliorating cognitive impairment in APP/PS1 transgenic mice by electroacupuncture
发布日期
2017-7-24作者
Liu, WL (Liu, Weilin)
Zhuo, PY (Zhuo, Peiyuan)
Li, L (Li, Long)
Jin, H (Jin, Hao)
Lin, BB (Lin, Bingbing)
Zhang, YZ (Zhang, Yingzheng)
Liang, SX (Liang, Shengxiang)
Wu, J (Wu, Jie)
Huang, J (Huang, Jia)
Wang, ZF (Wang, Zhifu)
Lin, RH (Lin, Ruhui)
Chen, LD (Chen, Lidian)
Tao, J (Tao, Jing)
所在专题
摘要
An essential feature of Alzheimer's disease (AD) is implicated in brain energy metabolic impairment that is considered underlying pathogenesis of cognitive impairment. Therefore, therapeutic interventions to allay cognitive deficits that target energy metabolism may be an efficacy strategy in AD. In this study, we found that electroacupuncture (EA) at the DU20 acupoint obviously increased glucose metabolism in specific brain regions such as cortex, hippocampus, cingulate gyrus, basal forebrain septum, brain stem, and cerebellum in APP/PS1 transgenic mice by animal F-18-Fluoro-2-deoxy-D-Glucose (F-18-FDG)/positron emission tomography (PET) imaging, accompanied by cognitive improvements in the spatial reference learning and memory and memory flexibility and novel object recognition performances. Further evidence shown energy metabolism occurred in neurons or non-neuronal cells of the cortex and hippocampus in terms of the co-location of GLUT3/NeuN and GLUT1/GFAP. Simultaneously, metabolic homeostatic factors were critical for glucose metabolism, including phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and AKT serine/threonine kinase. Furthermore, EA-induced phosphorylated AMPK and AKT inhibited the phosphorylation level of the mammalian target of rapamycin (mTOR) to decrease the accumulation of amyloid-beta (A beta) in the cortex and hippocampus. These findings are concluded that EA is a potential therapeutic target for delaying memory decline and A beta deposition of AD. The AMPK and AKT are implicated in the EA-induced cortical and hippocampal energy metabolism, which served as a contributor to improving cognitive function and A beta deposition in a transgenic mouse model of AD.
描述
通讯作者地址: Chen, LD; Tao, J (通讯作者)Fujian Univ Tradit Chinese Med, Coll Rehabil Med, Fuzhou 350122, Fujian, Peoples R China.
增强组织信息的名称 Fujian University of Traditional Chinese Medicine
地址:
[ 1 ] Fujian Univ Tradit Chinese Med, Coll Rehabil Med, Fuzhou 350122, Fujian, Peoples R China
[ 2 ] Fujian Key Lab Rehabil Technol, Fuzhou 350122, Fujian, Peoples R China
[ 3 ] Chinese Acad Sci, Inst High Energy Phys, Div Nucl Technol & Applicat, Beijing 100049, Peoples R China
电子邮件地址:cld@fjtcm.edu.cn; taojing01@163.com