Preventive Electroacupuncture Ameliorates D-Galactose-Induced Alzheimer's Disease-Like Pathology and Memory Deficits Probably via Inhibition of GSK3β/mTOR Signaling Pathway.

Chao-Chao Yu,Jia Wang,Jia Li,Bo-Cun Li,Shan Gao,Qing Shu,Wei Lu,Yan-Jun Du,Li Wang,Tao Jiang,Li-Hong Kong,Si-Si Ye,Xue-Song Wang

doi:10.1155/2020/1428752

Abstract

Acupuncture has been practiced to treat neuropsychiatric disorders for a thousand years in China. Prevention of disease by acupuncture and moxibustion treatment, guided by the theory of Chinese acupuncture, gradually draws growing attention nowadays and has been investigated in the role of the prevention and treatment of mental disorders such as AD. Despite its well-documented efficacy, its biological action remains greatly invalidated. Here, we sought to observe whether preventive electroacupuncture during the aging process could alleviate learning and memory deficits in D-galactose-induced aged rats. We found that preventive electroacupuncture at GV20-BL23 acupoints during aging attenuated the hippocampal loss of dendritic spines, ameliorated neuronal microtubule injuries, and increased the expressions of postsynaptic PSD95 and presynaptic SYN, two important synapse-associated proteins involved in synaptic plasticity. Furthermore, we observed an inhibition of GSK3β/mTOR pathway activity accompanied by a decrease in tau phosphorylation level and prompted autophagy activity induced by preventive electroacupuncture. Our results suggested that preventive electroacupuncture can prevent and alleviate memory deficits and ameliorate synapse and neuronal microtubule damage in aging rats, which was probably via the inhibition of GSK3β/mTOR signaling pathway. It may provide new insights for the identification of prevention strategies of AD.

Highlights

Alzheimer’s disease (AD), a neurodegenerative disease accounting for nearly 80% in all dementia diseases, is characterized by progressive memory decline, executive dysfunction, personality and behavioral changes, and other neuropsychiatric syndromes [1]
AD has become the most common cause of dementia, affecting a growing number of aging populations [3]. e prevalence of AD is increasing with the acceleration of global aging [48]
Intracellular NFTs accumulation as a result of tau hyperphosphorylation and aggregation is the early pathology in AD [10], and NFTs deposition can even be found in aging brains without obvious memory deficits [11]. erefore, prevention of neurofibrillary tangles accumulation as a result of tau hyperphosphorylation [49] and autophagy degradation deficits [50] may be a promising efficient intervention strategy for AD

Summary

Introduction

Alzheimer’s disease (AD), a neurodegenerative disease accounting for nearly 80% in all dementia diseases, is characterized by progressive memory decline, executive dysfunction, personality and behavioral changes, and other neuropsychiatric syndromes [1]. As the worldwide population ages, AD has become one of the most important medical and social problems in the world [4]. Since AD is insidious and its Evidence-Based Complementary and Alternative Medicine progression is difficult to reverse, it is of great significance to explore the early prevention strategy. Extracellular Aβ plaques and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau proteins in the cerebral cortex and hippocampus are the typical pathological changes of AD [2, 7]. It is well recognized that the severity of dementia is strongly correlated with NFTs rather than senile plaques [8, 9]. NFTs deposition as a result of tau hyperphosphorylation is recognized as the early pathological hallmark of AD [8, 10,11,12]. Paired helical filaments (PHFs) are the major component of NFTs [14, 15]

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