(-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease


BIBLIOGRAPHIC THERAPEUTIC AGENT ANIMAL MODEL EXPERIMENTAL DESIGN OUTCOMES

Bibliographic

Year of Publication:
2017
Contact PI Name:
Shuang Wang
Contact PI Affiliation:
Department of Pathophysiology, Institute of Basic Medicine Science, Xi’an Medical University, Xi’an, China
Co-Authors:
Yufang Guo, Yan Zhao, Ying Nan, Xiang Wang, Yulong Chen
Primary Reference (PubMED ID):
Funding Source:
Department of National Science and Technology of China
Natural Science Foundation of Shanxi Province of China
Study Goal and Principal Findings:

(-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic extract in green tea and it has attracted increasing attention for its multiple bioactive effects. However, the mechanisms by which EGCG exerts its neuroprotective actions in Alzheimer's disease (AD) are presently lacking. In the present study, a sporadic AD transgenic mouse model known as senescence-accelerated mouse prone 8 (SAMP8) was used to investigate whether oral administration of EGCG could improve recognition and memory function through reduction of amyloid β (Aβ) and tau hyperphosphorylation. Was also investigated the effects of chronic EGCG treatment on the synaptic dysfunction in the frontal cortex (FC) and the hippocampus (Hip) of AD mice. The results showed that long-term oral consumption of EGCG at a relatively high dose (15 mg/kg) improved memory function in SAMP8 mice in the Y-maze and Morris water maze. The levels of Aβ1-42 and BACE-1 in FC and Hip were significantly reduced by EGCG treatment. EGCG treatment also prevented the hyperphosphorylation of tau and reversed the decreased synaptic protein marker synaptophysin and postsynaptic density protein 95 in FC and Hip of SAMP8 mice. The present study suggests that long-term oral consumption of EGCG ameliorates impairments in spatial learning and memory and rescues the reduction in synaptic proteins observed in an AD mouse model. Thus, EGCG may represent a novel candidate agent for the treatment of neurodegenerative diseases.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Supplement
Therapeutic Agent:
(-)-Epigallocatechin-3-gallate
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Species:
Mouse
Model Type:
Accelerated Aging
Strain/Genetic Background:
Not Reported
Species:
Mouse
Model Type:
Accelerated Aging Resistant
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
Biomarkers
Dose
Formulation
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

Outcomes

Outcome Measured
Outcome Parameters
Behavioral
Morris Water Maze
Spontaneous Alternation
Y Maze
Motor Function
Locomotor Activity
Biochemical
Brain-beta Amyloid Peptide 42
beta-Site Amyloid Precursor Protein Cleaving Enzyme 1 (BACE1)
Synaptophysin
Postsynaptic Density Protein 95 (PSD95)
phospho-Tau
Toxicology
Body Weight

Source URL: http://alzped.nia.nih.gov/epigallocatechin-3-gallate-0