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Int J Clin Exp Pathol ; 8(7): 7710-28, 2015.
Article in English | MEDLINE | ID: mdl-26339337

ABSTRACT

Alzheimer's disease (AD) is a neurodegenerative disorder with progressive degeneration of the hippocampal and cortical neurons. This study was designed to demonstrate the protective effect of caffeine on gene expression of brain derived neurotrophic factor (BDNF) and its receptor neural receptor protein-tyrosine kinase-ß (TrkB) as well as glial fibrillary acidic protein (GFAP) and Ki-67 immunoreactivity in Aluminum chloride (AlCl3) induced animal model of AD. Fifty adult rats included in this study were classified into 5 group (10 rats each); negative and positive control groups (I&II), AD model group (III), group treated with caffeine from the start of AD induction (IV) and group treated with caffeine two weeks before AD induction (V). Hippocampal tissue BDNF and its receptor (TrkB) gene expression by real time RT-PCR in addition to immunohistochemical study of GFAP and Ki67 immunoreactivity were performed for all rats in the study. The results of this study revealed that caffeine has protective effect through improving the histological and immunohistochemical findings induced by AlCl3 as well as BDNF and its receptor gene expression. It could be concluded from the current study, that chronic caffeine consumption in a dose of 1.5 mg/kg body weight daily has a potentially good protective effect against AD.


Subject(s)
Alzheimer Disease/drug therapy , Brain-Derived Neurotrophic Factor/metabolism , Caffeine/pharmacology , Gene Expression Regulation/drug effects , Signal Transduction/drug effects , Aluminum Chloride , Aluminum Compounds/adverse effects , Alzheimer Disease/chemically induced , Alzheimer Disease/metabolism , Animals , Brain-Derived Neurotrophic Factor/genetics , Chlorides/adverse effects , Disease Models, Animal , Glial Fibrillary Acidic Protein/genetics , Glial Fibrillary Acidic Protein/metabolism , Hippocampus/drug effects , Hippocampus/pathology , Humans , Ki-67 Antigen/genetics , Ki-67 Antigen/metabolism , Male , Neurons/drug effects , Neurons/pathology , Rats , Rats, Sprague-Dawley , Receptor Protein-Tyrosine Kinases/genetics , Receptor Protein-Tyrosine Kinases/metabolism
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