Abstract
Neuroinflammation is considered as one of the crucial pathogenesis in promoting neurodegenerative progress of Alzheimer's disease (AD). As complementary and alternative therapy, electroacupuncture (EA) stimulation has been widely used in clinical practice for anti-inflammation. However, whether EA promotes the cognitive deficits resulting from neuroinflammation in AD remains unclear. In this study, the presenilin 1 and 2 conditional double knockout (PS cDKO) mice, exhibited a series of AD-like pathology, robust neuroinflammatory responses, and memory deficits, were used to evaluate the potential neuroprotective effect of EA at Baihui (GV 20) and Shenting (GV 24) by behavioral testing, electrophysiology recording, and molecular biology analyzing. First, we observed that EA improved memory deficits and impaired synaptic plasticity. Moreover, EA possesses an ability to suppress the hyperphosphorylated tau and robust elevated NLRP3, ASC, Caspase-1, IL-1β, and IL-18 in PS cDKO mice. Importantly, MCC950, a potent and selective inhibitor of NLPR3 inflammasome, has similar effects on inhibiting the hyperphosphorylated tau and the robust elevated NLRP3 components and neuroinflammatory responses of PS cDKO mice as well as EA treatment. Furthermore, EA treatment is not able to further improve the AD-like phenotypes of PS cDKO mice in combination with the MCC950 administration. Therefore, EA stimulation at GV 20 and GV 24 acupoints may be a potential alternative therapy for deterring cognitive deficits in AD through suppression of NLRP3 inflammasome activation.
Highlights
Alzheimer’s disease (AD) is the most common type of dementia in the elderly population [1], characterized by progressive decline in the cognitive and psychomotor function
We found that EA treatment ameliorated cognitive deficits, impaired longterm potentiation (LTP) induction, and abnormal expression of NMDA receptors of presenilin and conditional double knockout (PS cDKO) mice, which might be associated with the antineuroinflammatory effects of EA through blockage of the NLRP3 inflammasome signaling pathway in hippocampus
We found that 3 weeks EA stimulation at GV 20 and GV 24 acupoints could effectively ameliorate the memory deficits, improve the expression of NMDA receptors and LTP induction, inhibit hyperphosphorylated tau, and robust elevated neuroinflammatory responses in the PS cDKO mice
Summary
Alzheimer’s disease (AD) is the most common type of dementia in the elderly population [1], characterized by progressive decline in the cognitive and psychomotor function. Previous studies show that plagues, tangles, and neuronal debris persistently activate primed microglia, which results in a constant production of proinflammatory mediators, such as interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), nitric oxide, chemokines, and complements [5, 6]. These mediators maintain microglial activation and induce. Recent studies provide evidence that the NLRP3 inflammasome are essential for both the progression of Aβ and tau pathology directly in AD [12, 13] These findings indicate that NLRP3 inflammasome may be a potential therapeutic target for AD (or neurodegenerative disorders)
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