Electroacupuncture ameliorates cerebrovascular impairment in Alzheimer's disease mice via melatonin signaling. (15th November 2022)

• Record Type: Journal Article
• Authors: Jiang, Yimin; Lin, Yunshi; Tan, Yuhang; Shen, Xinkai; Liao, Meihua; Wang, Huan; Lu, Nannan; Han, Feng; Xu, Nenggui; Tang, Chunzhi; Song, Juxian; Tao, Rongrong
• Is Part Of: CNS neuroscience & therapeutics. Volume 29:Number 3(2023)
• Page Start: 917
• Page End: 931
• Publication Date: 2022-11-15
• Subjects: Alzheimer's disease -- cerebrovascular impairment -- electroacupuncture at ST36 acupoint -- endothelial cell -- melatonin signaling; Neuropharmacology -- Periodicals; Central nervous system -- Diseases -- Effect of drugs on -- Periodicals; 612.8
• DOI: 10.1111/cns.14027
• Languages: English
• ISSNs: 1755-5930

Abstract

Abstract: Aims: Cerebrovascular impairment contributes to the pathogenesis of Alzheimer's disease (AD). However, it still lacks effective intervention in clinical practice. Here, we investigated the efficacy of electroacupuncture (EA) in cerebrovascular repair in 3xTg‐AD mice and its mechanism. Methods: 3xTg‐AD mice were employed to evaluate the protective effect of EA at ST36 acupoint (EAST36). Behavioral tests were performed to assess neurological disorders. Laser speckle contrast imaging, immunostaining, and Western blot were applied to determine EAST36‐boosted cerebrovascular repair. The mechanism was explored in 3xTg mice and endothelial cell cultures by melatonin signaling modulation. Results: EAST36 at 20/100 Hz effectively alleviated the olfactory impairment and anxiety behavior and boosted cerebrovascular repair in AD mice. EAST36 attenuated cerebral microvascular degeneration in AD mice by modulating endothelial cell viability and injury. Consequently, the Aβ deposits and neural damage in AD mice were reversed after EAST36. Mechanistically, we revealed that EAST36 restored melatonin levels in AD mice. Melatonin supplement mimicked the EAST36 effect on cerebrovascular protection in AD mice and endothelial cell cultures. Importantly, blockage of melatonin signaling by antagonist blunted EAST36‐induced cerebrovascular recovery and subsequent neurological improvement. Conclusions: These findings provided strong evidence to support EAST36 as a potential nonpharmacological therapy against cerebrovascular impairment in AD. Further study is necessary to better understand how EAST36 treatment drives melatonin signaling. Abstract : Cerebrovascular protection has been recognized as an alternative target for Alzheimer's disease (AD) prevention and therapy based on the strong contribution of cerebrovascular dysfunction to AD progression. This work addressed that EA at ST36 (EAST36) works as an efficient approach to boost cerebrovascular repair and thereby neurological improvement against AD progression by activating melatonin signaling.