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(−)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice


Year of Publication:
Contact PI Name:
Minjie Wei
Contact PI Affiliation:
Department of Pharmacology, School of Pharmaceutical Sciences, China Medical University, Liaoning Province, China
Mingyan Liu, Fujun Chen, Lei Sha, Shuang Wang, Lin Tao, Lutian Yao, Miao He, Zhimin Yao, Hang Liu, Zheng Zhu, Zhenjie Zhang, Zhihong Zheng, Xianzheng Sha
Primary Reference (PubMED ID):
Funding Source:
Scientific Research Fund of Liaoning Provincial Education Department
Science and Technology Program of Liaoning Provence
National Science and Technology Major Special Project on Major New Drug Innovation of China
Study Goal and Principal Findings:

Epigallocatechin gallate (EGCG), also known as epigallocatechin-3-gallate, is a is a polyphenol, and  the most abundant catechin in green tea. EGCG has been found to possess potent iron chelating, antioxidant, anti-inflammatory and anti-oncogenic activities. Previous studies have reported that EGCG treatment significantly reduced Aβ generation in human-derived neuroblastoma (SH-SY5Y)  cell line, in murine neuron-like cells (N2a) transfected with human “Swedish” mutant APP, and in primary neurons derived from Swedish mutant APP-overexpressing mice (TgAPPsw line 2576). In addition, EGCG has been reported to markedly improve the cognitive deficits, APP processing, and Tau pathology in D-gal-induced AD mice, TgAPPsw line 2576 transgenic mice and PS2 transgenic mice. Taken together these studies suggest that that EGCG treatment is neuroprotective in some cell and animal models of Alzheimer’s disease (AD).

The goal of this study is to examine, the neuroprotective effects of EGCG on neurodegenerative pathology and behavioral deficits exhibited by APP/PS1 transgenic mice. The data found that EGCG treatment dramatically ameliorated the cognitive impairments, reduced the over expression of Aβ(1–40) and amyloid precursor protein (APP), and inhibited the neuronal apoptosis in  the APP/PS1 mice.   EGCG treatment reduced the number of Aβ and inhibited neuronal apoptosis oin the hippocampus.  Furthermore, EGCG treatment enhanced the relative expression level of NGF by increasing the NGF/pro-NGF ratio in the mice.  EGCG was also found to activate TrkA signaling by increasing the phosphorylation of TrkA following the increased phosphorylation of c-Raf, ERK1/2, and cAMP response element-binding protein (CREB).   Based on these data the authors suggest that EGCG is a potential therapeutic agent to provide beneficial effects on aging and AD.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Interventions & Supplements
Therapeutic Agent:
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Not Reported

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
Contextual Fear Conditioning
Morris Water Maze
Open Field Test
Amyloid Precursor Protein (APP)
Brain-beta Amyloid Peptide 40
Nerve Growth Factor (NGF)
Tyrosine Receptor Kinase A (TrkA)
phospho-Tyrosine Receptor Kinase A (phospho-TrkA)
Extracellular Signal-Regulated Kinase (ERK)
cAMP Response Element-Binding Protein (CREB)
c-Jun N-terminal Kinase 1/2 (JNK1/2)
Caspase Activation