Abstract

BackgroundAlzheimer’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.MethodsCognitive 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.ResultsEA 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.ConclusionsRepeated 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.

Highlights

  • Alzheimer’s disease (AD) is a severe neurodegenerative disease for which there is currently no effective treatment

  • We investigated whether EA treatment could ameliorate cognitive impairment and attenuate amyloid β-peptide (Aβ) deposits, and the effect of EA treatment on brain-derived neurotrophic factor (BDNF) expression and neurogenesis in the amyloid precursor protein (APP)/presenilin 1 (PS1) double transgenic (Tg) mice

  • Cognitive impairment and Aβ1-42 deposition presented in the Amyloid precursor protein/presenilin 1 (APP/PS1) mice Transgenic mice, which imitated the most salient characteristics of AD, were selected to simulate human Alzheimer’s disease

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Summary

Introduction

Alzheimer’s disease (AD) is a severe neurodegenerative disease for which there is currently no effective treatment. Prevalence is predicted to reach 80 million worldwide by 2040 [2]. Confronted with such a large number of people suffering from AD, the currently available treatments for the disease are limited and without. The pathology of AD is generally accepted as being characterized by the abnormally abundant deposition of amyloid plaques, neurofibrillary tangles, and selective neuronal loss in the frontal and temporal cortices, as well as the hippocampus of brain. A wealth of evidence has indicated that Aβ1-42 deposits participate in the process of neuron loss and lead to the occurrence of dementia in AD patients

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