Epigallocatechin-3-gallate Alleviates Cognitive Deficits in APP/PS1 Mice

Summary Alzheimer’s disease (AD) shows cognitive impairments in clinic, which is multifactorial with different etiopathogenic mechanisms such as Aβ deposition, neuroinflammation and neuronal dystrophy involved. Therefore, multi-targets drugs with neuroprotective, anti-amyloidogenic and anti-inflamma...

Full description

Saved in:
Bibliographic Details
Published inCurrent medical science Vol. 40; no. 1; pp. 18 - 27
Main Authors Bao, Jian, Liu, Wei, Zhou, Hong-yan, Gui, Yu-ran, Yang, You-hua, Wu, Meng-juan, Xiao, Yi-fan, Shang, Jin-ting, Long, Gui-feng, Shu, Xi-ji
Format Journal Article
LanguageEnglish
Published Wuhan Huazhong University of Science and Technology 01.02.2020
Department of Pathology and Pathophysiology, School of Medicine, Jianghan University, Wuhan 430056, China%Department of Traditional Chinese Medicine, School of Medicine, Jianghan University, Wuhan 430056, China%Department of Physiology, School of Medicine, Jianghan University, Wuhan 430056, China%Institutes of Biomedical Sciences, School of Medicine, Jianghan University, Wuhan 430056, China%School of Life Science, Jianghan University, Wuhan 430056, China
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Summary Alzheimer’s disease (AD) shows cognitive impairments in clinic, which is multifactorial with different etiopathogenic mechanisms such as Aβ deposition, neuroinflammation and neuronal dystrophy involved. Therefore, multi-targets drugs with neuroprotective, anti-amyloidogenic and anti-inflammatory properties will be effective in AD treatment. Epigallocatechin-3-gallate (EGCG) possesses a broad spectrum of pharmacological activities in the prevention and treatment of multiple neurodegenerative diseases. In the present study, we showed that oral administration of EGCG (50 mg/kg) for 4 months significantly attenuated the cognitive deficits in APP/PS1 transgenic mice, which served as AD model. Moreover, EGCG induced an improvement in dendritic integrity and expression levels of synaptic proteins in the brain of APP/PS1 mice. And EGCG exerted obvious anti-inflammatory effects, which was manifested by alleviating microglia activation, decreasing pro-inflammatory cytokine (IL-1β) and increasing anti-inflammatory cytokines (IL-10, IL-13). Furthermore, β-amyloid (Aβ) plaques were markedly reduced in the hippocampus of 6-month old APP/PS1 mice after EGCG treatment. In conclusion, these findings indicate that EGCG improves AD-like cognitive impairments through neuroprotective, anti-amyloidogenic and anti-inflammatory effects, thus is a promising therapeutic candidate for AD.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:2096-5230
1672-0733
2523-899X
1993-1352
DOI:10.1007/s11596-020-2142-z