Electroacupuncture Attenuates Learning and Memory Impairment via PI3K/Akt Pathway in an Amyloid β 25-35 -Induced Alzheimer's Disease Mouse Model.
Si-Mai ShaoKyung Hye ParkYe YuanZijuan ZhangYanwen YouZhenqiang ZhangLi HaoPublished in: Evidence-based complementary and alternative medicine : eCAM (2022)
The main characteristic of Alzheimer's disease (AD) is the progressive decline of learning and memory ability. Electroacupuncture (EA) may improve AD-related learning and memory ability. However, the underlying molecular mechanism of action remains unclear. The objective of the present study was to assess the effects and the molecular mechanism of EA on learning and memory in an amyloid β 25-35 (A β 25-35 ) induced AD mouse model. The AD model was established by intracerebroventricular (ICV) administration of A β 25-35 oligomers. AD mice were electroacupunctured with wisdom three-needle combined with Baihui (GV20) five times per week for three consecutive weeks. The Morris water maze (MWM) and Y maze tests were applied to evaluate spatial learning and memory ability. A transmission electron microscope (TEM) was used to measure mitochondria and autophagy of hippocampal neurons, and western blot was applied to observe molecular changes in the mice hippocampus. The results suggested that EA treatment significantly alleviated learning and memory impairment related to AD, reduced mitochondria damage, improved autophagy, increased mitochondrial protein 2 (Mfn2), Beclin 1, and LC3B, and decreased the expressions of fission protein 1 (Fis1) level. Furthermore, EA further upregulated the protein expression of phosphatidylinositol 3-kinase (PI3K) and the ratio of p-Akt/Akt in the hippocampus of AD mice. This study demonstrates that EA treatment attenuates cognitive deficits, modulates mitochondrial fusion and fission, and enhances autophagy via the PI3K/Akt pathway in a mouse AD model.
Keyphrases
- oxidative stress
- mouse model
- cell death
- signaling pathway
- diabetic rats
- endoplasmic reticulum stress
- cerebral ischemia
- cell proliferation
- high fat diet induced
- cognitive decline
- drug induced
- neuropathic pain
- reactive oxygen species
- adipose tissue
- insulin resistance
- amino acid
- protein protein
- subarachnoid hemorrhage
- combination therapy
- high resolution
- endoplasmic reticulum
- prefrontal cortex
- replacement therapy