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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 am...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907495/ https://www.ncbi.nlm.nih.gov/pubmed/24447795 http://dx.doi.org/10.1186/1472-6882-14-37 |
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author | Li, Xuying Guo, Fan Zhang, Qiaomei Huo, Tingting Liu, Lixin Wei, Haidong Xiong, Lize Wang, Qiang |
author_facet | Li, Xuying Guo, Fan Zhang, Qiaomei Huo, Tingting Liu, Lixin Wei, Haidong Xiong, Lize Wang, Qiang |
author_sort | Li, Xuying |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3907495 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-39074952014-01-31 Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice Li, Xuying Guo, Fan Zhang, Qiaomei Huo, Tingting Liu, Lixin Wei, Haidong Xiong, Lize Wang, Qiang BMC Complement Altern Med Research Article 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. BioMed Central 2014-01-22 /pmc/articles/PMC3907495/ /pubmed/24447795 http://dx.doi.org/10.1186/1472-6882-14-37 Text en Copyright © 2014 Li et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Li, Xuying Guo, Fan Zhang, Qiaomei Huo, Tingting Liu, Lixin Wei, Haidong Xiong, Lize Wang, Qiang Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title | Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title_full | Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title_fullStr | Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title_full_unstemmed | Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title_short | Electroacupuncture decreases cognitive impairment and promotes neurogenesis in the APP/PS1 transgenic mice |
title_sort | electroacupuncture decreases cognitive impairment and promotes neurogenesis in the app/ps1 transgenic mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907495/ https://www.ncbi.nlm.nih.gov/pubmed/24447795 http://dx.doi.org/10.1186/1472-6882-14-37 |
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