"Olfactory three-needle" acupuncture enhances synaptic function in Aβ1-42-induced Alzheimer's disease via activating PI3K/AKT/GSK-3β signaling pathway.

Abstract

Synaptic dysfunction and neuronal loss are related to cognitive impairment of Alzheimer's disease. Recent evidence indicates that regulating the phosphatidylinositol 3-Kinase (PI3K)/AKT/GSK-3β pathway is a therapeutic strategy for improving synaptic plasticity in Alzheimer's disease. Here, we investigated "olfactory three-needle" effects on synaptic function and the PI3K/AKT/GSK-3β signaling pathway in β-amyloid1-42 (Aβ1-42)-induced Alzheimer's disease rats. A three-needle olfactory bulb insertion for 28 days alleviated Aβ1-42-induced Alzheimer's disease rats' cognitive impairment as assessed by performance in the Morris water maze test. Furthermore, the three-needle electrode inhibited neuro-apoptosis and neuro-inflammation. It significantly upregulated the protein expression of postsynaptic density protein 95, synaptophysin, and GAP43, indicating a protective effect on hippocampal synaptic plasticity. Additionally, the activation level of PI3K/AKT signaling and the phosphorylation inactivation of GSK-3β were significantly enhanced by the "olfactory three-needle". Our findings suggested that the three-needle acupuncture is a potential alternative to improve synaptic plasticity and neuronal survival of Alzheimer's disease brain in rodents.

• Authors: Yuan Wang, Ani Zheng, Huan Yang, Qiang Wang, Bo Ren, Ting Guo, Jing Qiang, Hui Cao, Yu-Jie Gao, Lei Xu, Hui Li, Ling He, Zhi-Bin Liu
• Journal: Journal of integrative neuroscience (J Integr Neurosci) Vol. 20 Issue 1 Pg. 55-65 (Mar 30 2021) ISSN: 0219-6352 [Print] Singapore
• PMID: 33834691 (Publication Type: Journal Article)
• Copyright: © 2021 The Authors. Published by IMR Press.

Chemical References

• Amyloid beta-Peptides
• Peptide Fragments
• amyloid beta-protein (1-42)
• Glycogen Synthase Kinase 3 beta
• Oncogene Protein v-akt

Topics

• Acupuncture Therapy
• Alzheimer Disease (chemically induced, complications, therapy)
• Amyloid beta-Peptides (pharmacology)
• Animals
• Apoptosis (physiology)
• Behavior, Animal (physiology)
• Cognitive Dysfunction (etiology, therapy)
• Glycogen Synthase Kinase 3 beta (metabolism)
• Inflammation (therapy)
• Male
• Maze Learning (physiology)
• Neuronal Plasticity (physiology)
• Olfactory Bulb
• Oncogene Protein v-akt (metabolism)
• Peptide Fragments (pharmacology)
• Phosphatidylinositol 3-Kinases (metabolism)
• Rats
• Rats, Sprague-Dawley
• Signal Transduction (physiology)