Effect of the electro-acupuncture on senile plaques and its formation in APP+/PS1+ double transgenic mice

Genes Dis. 2018 Jun 15;6(3):282-289. doi: 10.1016/j.gendis.2018.06.002. eCollection 2019 Sep.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease and its incidence will increase with age and is aggravating. The senile plaques (SPs) are one of three main pathological features in AD patients, which are formed by amyloid β-protein (Aβ) over-accumulation. β-amyloid precursor protein (APP), β-site APP cleavage (BACE1), and insulin degrading enzyme (IDE) proteins participate in the process of Aβ production and degradation. At present, the pathogenesis of AD is not yet clear and the current treatment methods can only relief the related symptoms of AD. The electro-acupuncture (EA) is a traditional Chinese medicine treatment combined the acupuncture and electrical stimulation and the treatment effect can also be controlled by transform the electrical frequency. Thus, in this experiment, we carried out behavioral test, immunohistochemistry (IHC), and Western Blot (WB) after different period treatments to the model mice by electro-acupuncturing "Baihui" and "Shenshu" acupoints in APP+/PS1+ double transgenic mice. It was found that the EA therapy can improve the ability of learning, memory and spatial exploration, and reduce the deposition of SPs in brain of AD model mice, and reduce the expressions of APP and BACE1, increase the expression of IDE protein. These results prompt that EA can effectively alleviate the pathological process of AD. We speculate that EA may play a comprehensive role in preventing the development of AD, considering the previous data.

Keywords: AD, Alzheimer's disease; APP, β-; Ach, aetylcholine; AchE, cholinesterase; Alzheimer's disease; Amyloid β-protein; Aβ, amyloid β-protein; ChAT, aetylcholine tansferase; EA, electro-acupuncture; Electro-acupuncture; IDE, insulin degrading enzyme; IHC, immunohistochemistry; SOD, superoxide dismutase; SPs, senile plaques; Senile plaques; Transgenic mice; amyloid precursor protein, BACE1; β-, site APP cleavage.