Mechanisms of Electroacupuncture on Alzheimer's Disease: A Review of Animal Studies.
10.1007/s11655-020-3092-9
- Author:
Yang-Yang SONG
1
;
Wen-Tao XU
1
;
Xin-Chang ZHANG
1
;
Guang-Xia NI
2
,
3
Author Information
1. College of Acupuncture and Massage, College of Regimen and Rehabilitation, Nanjing University of Traditional Chinese Medicine, Nanjing, 210023, China.
2. College of Acupuncture and Massage, College of Regimen and Rehabilitation, Nanjing University of Traditional Chinese Medicine, Nanjing, 210023, China. xgn66@
3. com.
- Publication Type:Journal Article
- Keywords:
Alzheimer’s disease;
Chinese medicine;
electroacupuncture;
mechanism
- From:
Chinese journal of integrative medicine
2020;26(6):473-480
- CountryChina
- Language:English
-
Abstract:
Alzheimer's disease (AD) is the main type of dementia affecting elderly people. The medicines used for treating AD have limits in their ability to alleviate cognitive and functional decline. Electroacupuncture (EA), an economical alternative and complementary therapeutic measure used in Chinese medicine, has strong clinical applicability, and its treatment effects are more reliable as its stimulation factors can be standardized. EA has been effectively used for ameliorating spatial learning and memory impairment in AD patients and rodent AD models. Here, we summarized the mechanisms of EA on rodent AD models, aiming to provide a theoretical basis for identifying new targets and research directions, and exploring appropriate EA stimulation parameters, then provide a detailed methodology to optimize the effects of EA, ultimately reducing the heavy burden of treating AD patients on families and countries. Our review showed that 8 acupoints were used when treating AD animals; Baihui (GV 20) was the most frequently used. Four mechanisms of EA were studied: (1) protection of cerebral neurons from oxidative stress, apoptosis, neuroinflammation, synaptic plasticity and hormone levels; (2) regulation of metabolism, including glucose metabolism and plasma metabolism; (3) regulation of brain-derived neurotrophic factor; and (4) regulation of β-amyloid peptide protein deposition.
