Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice.
BACKGROUND
Alzheimer's disease (AD) is a severe neurodegenerative disease for which there is currently no effective treatment. The purpose of this study was to investigate whether repeated electroacupuncture (EA) stimulation would improve cognitive function and the pathological features of AD in amyloid precursor protein (APP)/presenilin 1 (PS1) double transgenic mice.


METHODS
Cognitive function of APP/PS1 double transgenic mice was assessed using the Morris water maze test before and after EA treatment. Levels of amyloid β-peptide (Aβ) deposits in the hippocampus and cortex were evaluated by immunofluorescence, western blot and enzyme-linked immunosorbent assay. Expression of brain-derived neurotrophic factor (BDNF) was also examined by immunofluorescence and western blot. The neurogenesis was labeled by the DNA marker bromodeoxyuridine.


RESULTS
EA stimulation significantly ameliorated the learning and memory deficits of AD mice by shortening escape latency and increasing the time spent in the target zone during the probe test. Additionally, decreased Aβ deposits and increased BDNF expression and neurogenesis in the hippocampus and cortex of EA-treated AD mice were detected. The same change was detected in wild-type mice after EA treatment compared with wild-type mice without EA treatment.


CONCLUSIONS
Repeated EA stimulation may improve cognitive function, attenuate Aβ deposits, up-regulate the expression of BDNF and promote neurogenesis in the APP/PS1 double transgenic mice. This suggests that EA may be a promising treatment for AD.
Xuying
X
Li
Fan
F
Guo
Qiaomei
Q
Zhang
Tingting
T
Huo
Lixin
L
Liu
Haidong
H
Wei
Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, Shaanxi Province, China. lxiong@fmmu.edu.cn.
Lize
L
Xiong
Qiang
Q
Wang
D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D003071:Cognition; D003072:Cognition Disorders / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D004195:Disease Models, Animal; D015671:Electroacupuncture; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D018782:Maze Learning; D008569:Memory Disorders / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D055495:Neurogenesis; D053764:Presenilin-1 / Q000235:genetics / Q000378:metabolism
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D019208:Brain-Derived Neurotrophic Factor; D053764:Presenilin-1; C580804:presenilin 1, mouse