ArticleBiochemical genetics2024
Electroacupuncture Improves Learning and Memory Abilities via Activating AMPK/mTOR-Induced Autophagy in APP/PS1 Mice.
Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Electroacupuncture inhibited neuronal apoptosis through PGAM5/FUNDC1-dependent mitophagy after ischemic stroke.Chinese medicine · 2026Article
- Electroacupuncture in the treatment of non-alcoholic fatty liver disease: mechanistic insights and therapeutic potential.Frontiers in medicine · 2026Review
- The Mechanism of Acupuncture Regulating Autophagy: Progress and Prospect.Biomolecules · 2025Review
- Acupuncture for neurodegenerative diseases: mechanisms, efficacy, and future research directions.American journal of translational research · 2025Review
- Study on the Effects of Acupuncture with the "Yizhi Tiaoshen" Acupoint Formula on Blood Oxygen Metabolism and Neural Function in Key Brain Regions of AD Rats.Degenerative neurological and neuromuscular disease · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) has become a global public health problem characterized by memory and cognitive impairments. Electroacupuncture (EA) has been indicated to exert promising therapeutic effects on AD. This study aimed to further investigate the underlying mechanism of EA in AD treatment. APP/PS1 transgenic mice and wide-type mice underwent with or without EA treatment at GV20 and BL23 acupoints. Morris water maze test was utilized for examining the learning and memory of mice. Hematoxylin-eosin, Congo red, immunofluorescence, and TUNEL staining were employed for detecting the pathological changes of mouse brain hippocampus. Western blotting was implemented for measuring protein levels of autophagy- and AMPK/mTOR pathway-associated markers. APP/PS1 mice exhibited significant impairments in the spatial learning and memory. EA treatment improved the cognitive impairments, reduced amyloid-beta (Aβ) deposition, and alleviated neuronal apoptosis in the hippocampal tissues of APP/PS1 mice. EA promoted autophagy and activated the AMPK/mTOR signaling pathway in the hippocampus of APP/PS1 mice. EA improves the cognitive deficits, enhances Aβ clearance, and attenuates neuronal apoptosis in APP/PS1 mice in part by activating AMPK/mTOR-mediated autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.