PMID- 24447795
OWN - NLM
STAT- MEDLINE
DCOM- 20151008
LR  - 20211021
IS  - 1472-6882 (Electronic)
IS  - 1472-6882 (Linking)
VI  - 14
DP  - 2014 Jan 22
TI  - Electroacupuncture decreases cognitive impairment and promotes neurogenesis in 
      the APP/PS1 transgenic mice.
PG  - 37
LID - 10.1186/1472-6882-14-37 [doi]
AB  - 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 beta-peptide (Abeta) 
      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 Abeta 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 Abeta 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.
FAU - Li, Xuying
AU  - Li X
FAU - Guo, Fan
AU  - Guo F
FAU - Zhang, Qiaomei
AU  - Zhang Q
FAU - Huo, Tingting
AU  - Huo T
FAU - Liu, Lixin
AU  - Liu L
FAU - Wei, Haidong
AU  - Wei H
FAU - Xiong, Lize
AU  - Xiong L
AD  - Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical 
      University, Xi'an 710032, Shaanxi Province, China. lxiong@fmmu.edu.cn.
FAU - Wang, Qiang
AU  - Wang Q
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140122
PL  - England
TA  - BMC Complement Altern Med
JT  - BMC complementary and alternative medicine
JID - 101088661
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Presenilin-1)
RN  - 0 (presenilin 1, mouse)
SB  - IM
MH  - Alzheimer Disease/metabolism/pathology/*therapy
MH  - Amyloid beta-Peptides/*metabolism
MH  - Amyloid beta-Protein Precursor/genetics/metabolism
MH  - Animals
MH  - Brain/*metabolism
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cognition
MH  - Cognition Disorders/etiology/metabolism/*therapy
MH  - Disease Models, Animal
MH  - *Electroacupuncture
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Maze Learning
MH  - Memory Disorders/etiology/metabolism/*therapy
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - *Neurogenesis
MH  - Presenilin-1/genetics/metabolism
PMC - PMC3907495
EDAT- 2014/01/23 06:00
MHDA- 2015/10/09 06:00
PMCR- 2014/01/22
CRDT- 2014/01/23 06:00
PHST- 2013/05/18 00:00 [received]
PHST- 2014/01/10 00:00 [accepted]
PHST- 2014/01/23 06:00 [entrez]
PHST- 2014/01/23 06:00 [pubmed]
PHST- 2015/10/09 06:00 [medline]
PHST- 2014/01/22 00:00 [pmc-release]
AID - 1472-6882-14-37 [pii]
AID - 10.1186/1472-6882-14-37 [doi]
PST - epublish
SO  - BMC Complement Altern Med. 2014 Jan 22;14:37. doi: 10.1186/1472-6882-14-37.