Author/Authors :
Mahmoodzadeh، Tahereh نويسنده Department of Anatomy, School of Biology, Damghan University, Damghan, IR Iran , , Haji Khasem Kashani، Maryam نويسنده Damghan University, Damghan, IR Iran , , Ramshini، Hassan نويسنده Biology Department, Payam Noor University, 19395-4697 Tehran, I.R. of Iran Ramshini, Hassan , Moslem، Alireza نويسنده Department of Sciences, School of Nursing & Midwifery, Mashhad University of Medical Sciences, Mashhad , , Mohammad-Zadeh، Mohammad نويسنده Cellular and Molecular Research Center, Department of Physiology & Pharmacology, School of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran. Mohammad-Zadeh, Mohammad
Abstract :
Background
Alzheimer’s disease (AD) is one of the most common types of neurodegenerative disorders. The accumulation of Aβ plaques in the hippocampus contributes primarily to memory impairment. Green tea polyphenols prevent brain aging.
Objectives
In this study, green tea extract was used to prevent the generation of Aβ plaques in a rat model of AD induced by hen egg white lysozyme (HEWL).
Materials and Methods
Rats (n = 36) weighing 250 - 280 g were divided into six groups: control and positive control groups received normal saline and scopolamine, respectively; the lesion group received HEWL; and the treated groups received a mixture of HEWL and green tea extract at three doses into the hippocampus. Twenty days after injection, spatial memory was assessed by Morris water maze.
Results
Treated rats showed a significant decrease in escape latency, compared with lesion and positive control groups, indicating improvement in spatial memory. The AD groups showed significant decrease in escape latency than the control group, indicating impairment of spatial memory. Histological analysis revealed more number of Aβ plaques in the hippocampus of the injured group than that in the treated animals.
Conclusions
Our results suggest that the green tea extract is effective in preventing amyloid fibril formation and lysozyme fibrillization that in turn results in the improvement of memory deficits in the rat model of AD.
