Abstract
Microglia are the primary cells that exert immune function in the central nervous system, and accumulating evidence suggests that microglia act as critical players in the initiation of neurodegenerative disorders, such as Alzheimer's disease (AD). Microglia seemingly demonstrate two contradictory phenotypes in response to different microenvironmental cues, the M1 phenotype and the M2 phenotype, which are detrimental and beneficial to pathogenesis, respectively. Inhibiting the M1 phenotype with simultaneous promoting the M2 phenotype has been suggested as a potential therapeutic approach for cure AD. In this study, we demonstrated that electroacupuncture at the Shenting and Baihui acupoints for 16 weeks could improve learning and memory in the Morris water maze test and reduce amyloid β-protein in the parietal association cortex and entorhinal cortex in mice with mild and moderate AD. Besides, electroacupuncture at the Shenting and Baihui acupoints not only suppressed M1 marker (iNOS/IL-1β) expression but also increased the M2 marker (CD206/Arg1) expression in those regions. We propose that electroacupuncture at the Shenting and Baihui acupoints could regulate microglial polarization and decrease Aβ plaques to improve learning and memory in mild AD mice.
Highlights
Alzheimer’s disease (AD) is an age-related neurodegenerative disease that has become the fourth leading cause of death worldwide [1]
In mild AD, the escape latency was decreased (P < 0:01, Figure 1(a)), and the number of platform crossings was increased (P < 0:05, Figure 1(b)) in the WT group compared with the AD group in the Morris water maze (MWM) test
There was no significant difference between the AD group, the EA group, and the NA group at baseline
Summary
Alzheimer’s disease (AD) is an age-related neurodegenerative disease that has become the fourth leading cause of death worldwide [1]. Microglia have complex roles that are detrimental and beneficial to AD pathogenesis: M1 phenotypes are characterized by the production of inducible nitric oxide synthase (iNOS) and inflammatory cytokines (such as IL-1β) and damage healthy cells, such as neurons, leading to Aβ accumulation; M2 phenotypes express mannose receptor (CD206) and arginase 1 (Arg1) and downregulate neuroinflammation and remove Aβ plaques. The ablation of iNOS in APP/PS1 mice can protect mice from the plaque formation and premature mortality [20] These contradictory functions of microglia reflect their acquisition of distinct M1/M2 phenotypes in response to different microenvironmental cues [21, 22]. We chose 4- and 12-month-old APP/PS1 mice to simulate mild AD and moderate AD, respectively, aiming to investigate whether EA could regulate the microglial polarization to modulate learning and memory at different stages of Alzheimer’s disease
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