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(-)-Epigallocatechin-3-gallate ameliorates learning and memory impairments by attenuating peroxidation in APP/PS1 transgenic mice

Authors
Journal
Molecular Neurodegeneration
1750-1326
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Volume
7
Identifiers
DOI: 10.1186/1750-1326-7-s1-s29
Keywords
  • Meeting Abstract
Disciplines
  • Biology
  • Medicine

Abstract

(-)-Epigallocatechin-3-gallate ameliorates learning and memory impairments by attenuating peroxidation in APP/PS1 transgenic mice MEETING ABSTRACT Open Access (-)-Epigallocatechin-3-gallate ameliorates learning and memory impairments by attenuating peroxidation in APP/PS1 transgenic mice Mingyan Liu, Fujun Chen, Tao Lin, Lutian Yao, Miao He, Zheng Zhu, Zhimin Yao, Shuang Wang, Weifan Yao, Zhenjie Zhang, Qiushi Tang, Minjie Wei* From 2011 International Conference on Molecular Neurodegeneration Shanghai, China. 22-24 September 2011 Background Alzheimer’s disease (AD), an age-related neurodegenera- tive disorder, is the predominant form of dementia in the elderly, clinically characterized by cognitive impair- ment and pathologically characterized by extracellular senile plaques largely composed of b-amyloid (Ab) pep- tide. The overburden of b-amyloid (Ab) deposition in AD is associated with peroxidation which plays an important role in neuronal dysfunction. APP/PS1 double transgenic mice, which display significant learning and memory impairments and the typical pathological changes such as numerous Ab deposition, are ideal model to mimic the symptoms of AD. (-)-Epigallocate- chin-3-gallate (EGCG) is the most abundant polypheno- lic constituent in green tea, which has ironchelating, anti-inflammatory, antioxidant and anticancer activities. However, it remains unclear whether EGCG improves learning and memory impairments by attenuating perox- idation in APP/PS1 double transgenic mice. Therefore, we evaluated the relationships between the ameliorated memory dysfunctions and the inhibited peroxidative levels in APP/PS1 transgenic mice after EGCG treatment. Methods APP/PS1 mice at the age of 9 months, randomly distrib- uted into EGCG-treated APP/PS1 group (EGCG group) or APP/PS1 group, and age-matched wild-type mice (C57 BL/6J, WT group) were assigned as aging control. Mice were intragastrically administered EGCG (2 mg/ kg) or vehicle (distilled water) once daily for 4 weeks. Memory

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