Abstract
Alzheimer’s disease (AD), as one of most common dementia, mainly affects older people from the worldwide. In this study, we intended to explore the possible mechanism of improving cognitive function and protecting the neuron effect by electroacupuncture. Method: We applied senescence-accelerated mouse prone 8 (SAMP8) mice as AD animal model, used Morris water maze, HE staining, 16S rDNA amplicon sequencing of gut microbiota and ELISA to demonstrate our hypothesis. Results: electroacupuncture improved the learning and memory abilities in SAMP8 mice (P<0.05) and could protect the frontal lobe cortex and hippocampus of SAMP8 mice; electroacupuncture significantly decreased the expression of IL-1β (P<0.01), IL-6 (P<0.01) and TNF-α (P<0.01 in hippocampus, P<0.05 in serum) in serum and hippocampus; electroacupuncture balanced the quantity and composition of gut microbiome, especially of the relative abundance in Delta-proteobacteria (P<0.05) and Epsilon-proteobacteria (P<0.05). Conclusion: electroacupuncture treatment could inhibit the peripheral and central nerve system inflammatory response by balancing the gut microbiota.
Highlights
Alzheimer’s disease (AD), as one of most common dementia, which mainly affects elderly people, gains more and more awareness from the worldwide
The senile plaques (SPs) formed by deposition of amyloid-β protein [2] and neurofibrillary tangles (NFTs) formed by hyperphosphorylation of tau protein [3] were viewed as the characteristics of AD, and the neuroinflammatory reaction participated by glial cells were viewed as the key pathological changes of AD [4]
The shortening of escape latency was the most obvious in control group; compared with AD group, the escape time was significantly shortened from the third day to the fifth day (P
Summary
Alzheimer’s disease (AD), as one of most common dementia, which mainly affects elderly people, gains more and more awareness from the worldwide. According to the survey of Alzheimer’s disease International (ADI), there are over 9.9 million new cases of dementia each year worldwide, implying one new case every 3.2 seconds [1]. Since researchers first recognized this disease, they never stopped to find the pathological process and explore the effective therapies. The senile plaques (SPs) formed by deposition of amyloid-β protein [2] and neurofibrillary tangles (NFTs) formed by hyperphosphorylation of tau protein [3] were viewed as the characteristics of AD, and the neuroinflammatory reaction participated by glial cells were viewed as the key pathological changes of AD [4]. There are still no effectiveness therapies, which could reverse or terminate the process of the disease [5].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
