Electroacupuncture Enhances Cognition by Promoting Brain Glucose Metabolism and Inhibiting Inflammation in the APP/PS1 Mouse Model of Alzheimer’s Disease: A Pilot Study
Affiliations: [a] School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China
| [b] Department of Rehabilitation and Traditional Chinese Medicine, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
| [c] Information Engineering Institute, Beijing Institute of Graphic Communication, Beijing, China
| [d] Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China
Correspondence:
[*]
Correspondence to: Anping Xu, School of Acupuncture-moxibustion and Tuina, Beijing University of Chinese
Medicine, Beijing, 100029, China. E-mail: xuanping01@163.com.
Abstract: Background:Alzheimer’s disease (AD) is a neurodegenerative disease, yet there is no effective treatment. Electroacupuncture (EA) is a complementary alternative medicine approach. In clinical and animal studies, EA promotes cognition in AD and vascular dementia. It has been previously reported that cognitive decline in AD might be closely related to reduced glucose intake in the brain. It is worth mentioning that the regions of glucose hypometabolism are usually found to be associated with neuroinflammation. Objective:This study is to explore whether the protective mechanism of EA on cognition is related to the regulation of glucose metabolism and neuroinflammation. Methods:APP/PS1 mice were randomly divided into AD group and the treatment (AD + EA) group. In the AD + EA group, EA was applied on Baihui (GV20) and Yintang (GV29) for 20 min and then pricked at Shuigou (GV26), once every alternate day for 4 weeks. Morris water maze (MWM) tests were performed to evaluate the effects of EA treatment on cognitive functions. 18F-FDG PET, immunofluorescence, and western blot were used to examine the mechanisms underlying EA effects. Results:From MWM tests, EA treatment significantly improved cognition of APP/PS1 mice. From the 18F-FDG PET, the levels of uptake rate of glucose in frontal lobe were higher than the AD group after EA. From immunofluorescence and western blot, amyloid-β (Aβ) and neuroinflammation were reduced after EA. Conclusion:These results suggest that EA may prevent cognitive decline in AD mouse models by enhancing glucose metabolism and inhibiting inflammation-mediated Aβ deposition in the frontal lobe.
