Abstract
Alzheimer's disease (AD) is one of the most serious public health concerns facing the world. Its characteristic feature is neuroinflammation due to microglial activation. Electroacupuncture is one of the therapies employed to improve the condition of patients with AD, although its mechanism of action is still to be determined. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglia-specific receptor that is involved in regulating neuroinflammation in AD. In this study, we applied senescence-accelerated mouse-prone 8 mice as the AD animal model, used the Morris water maze, and applied hematoxylin and eosin staining, immunofluorescence double staining, and Western blotting, to explore the effects and potential mechanisms of action of electroacupuncture. In summary, this study suggested that electroacupuncture treatment could improve the learning and memory abilities (p < 0.05) and protect neurons. These effects result from acupuncture could upregulate TREM2 expression in the hippocampus (p < 0.01), which was essential for the anti-inflammatory effects in the AD animal model. However, further studies are needed to conclusively demonstrate the mechanism of action of electroacupuncture in AD.
Highlights
As the commonest cause of dementia, Alzheimer’s disease (AD) is a growing global health concern with huge implications for individuals and society [1]
We investigated whether acupuncture therapy improved AD by regulating the expression of Triggering receptor expressed on myeloid cells 2 (TREM2) on microglia using a recognized AD animal model
Eight-month-old senescence-accelerated mouse-prone 8 (SAMP8) mice [15] and senescenceaccelerated mouse-resistant 1 (SAMR1) mice weighing 30:0 ± 2:0 g were purchased from the Experimental Animal Center of the First Teaching Hospital of Tianjin University of Traditional Chinese Medicine (Animal Lot: SCXK (Jing) 2014-0003)
Summary
As the commonest cause of dementia, Alzheimer’s disease (AD) is a growing global health concern with huge implications for individuals and society [1]. This neurodegenerative disease is characterized classically by two hallmark pathologies: β-amyloid plaque deposition and neurofibrillary tangles of hyperphosphorylated tau [2]. There is increasing evidence for researchers to consider brain neuroinflammation as a new feature of AD [3], which is associated with microglial activation [4]. Excessive microglial activation damages the surrounding healthy neural tissue, and the factors secreted by the dead or dying neurons in turn exacerbate the chronic activation of microglia, causing progressive loss of neurons [7]. More researchers direct their energies into determining the mechanism of regulating microglial activation in AD
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