cytochrome-c-t and Learning-Disabilities

cytochrome-c-t has been researched along with Learning-Disabilities* in 1 studies

Other Studies

1 other study(ies) available for cytochrome-c-t and Learning-Disabilities

Article	Year
Dexamethasone and Aβ₂₅-₃₅ accelerate learning and memory impairments due to elevate amyloid precursor protein expression and neuronal apoptosis in 12-month male rats. Behavioural brain research, 2012, Feb-01, Volume: 227, Issue:1 Alzheimer's disease (AD) is an irreversible, progressive brain disorder of the elderly characterized by learning and memory impairment. Stress level glucocorticoids (GCs) and β-amyloid (Aβ) peptides deposition are found to be correlated with dementia progression in patients with AD. However, little is known about the simultaneous effects of glucocorticoids and Aβ on learning and memory impairment and its mechanism. In this study, 12-month-old male rats were chronically treated with Aβ(25-35) (10 μg/rat, hippocampal CA1 injection) and dexamethasone (DEX, 1.5mg/kg) for 14 days to investigate the effects of DEX and Aβ(25-35) treatment on learning and memory impairments, pathological changes, neuronal ultrastructure, amyloid precursor protein (APP) processing and neuronal cell apoptosis. Our results showed that DEX or Aβ(25-35) treatment alone for 14 days had caused slight damage on learning and memory impairments and hippocampal neurons, but damages were significantly increased with DEX+Aβ(25-35) treatment. And the mRNA levels of the APP, β-secretase and caspase 3 were significantly increased after DEX+Aβ(25-35) treatment. The immunohistochemistry demonstrated that APP, Aβ(1-40), caspase 3 and cytochrome c in hippocampus CA1 were significantly increased. Furthermore, Hoechst 33258 staining and Aβ(1-40) ELISA results showed that DEX+Aβ(25-35) treatment induced hippocampus CA1 neuron apoptosis and increased the level of Aβ(1-40). The results suggest that the simultaneous effects of GCs and Aβ may have important roles in the etiopathogenesis of AD, and demonstrate that stressful life events and GC therapy may increase the toxicity of Aβ and have cumulative impacts on the course of AD development and progression. Topics: Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; Analysis of Variance; Animals; Apoptosis; Arabidopsis Proteins; Caspase 3; Cytochromes c; Dexamethasone; Disease Models, Animal; Drug Synergism; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Glucocorticoids; Hippocampus; Intramolecular Transferases; Learning Disabilities; Male; Maze Learning; Memory Disorders; Microscopy, Electron, Scanning; Neurons; Peptide Fragments; Rats; Rats, Sprague-Dawley; Time Factors	2012

Article

Year

Dexamethasone and Aβ₂₅-₃₅ accelerate learning and memory impairments due to elevate amyloid precursor protein expression and neuronal apoptosis in 12-month male rats.

Behavioural brain research, 2012, Feb-01, Volume: 227, Issue:1

Alzheimer's disease (AD) is an irreversible, progressive brain disorder of the elderly characterized by learning and memory impairment. Stress level glucocorticoids (GCs) and β-amyloid (Aβ) peptides deposition are found to be correlated with dementia progression in patients with AD. However, little is known about the simultaneous effects of glucocorticoids and Aβ on learning and memory impairment and its mechanism. In this study, 12-month-old male rats were chronically treated with Aβ(25-35) (10 μg/rat, hippocampal CA1 injection) and dexamethasone (DEX, 1.5mg/kg) for 14 days to investigate the effects of DEX and Aβ(25-35) treatment on learning and memory impairments, pathological changes, neuronal ultrastructure, amyloid precursor protein (APP) processing and neuronal cell apoptosis. Our results showed that DEX or Aβ(25-35) treatment alone for 14 days had caused slight damage on learning and memory impairments and hippocampal neurons, but damages were significantly increased with DEX+Aβ(25-35) treatment. And the mRNA levels of the APP, β-secretase and caspase 3 were significantly increased after DEX+Aβ(25-35) treatment. The immunohistochemistry demonstrated that APP, Aβ(1-40), caspase 3 and cytochrome c in hippocampus CA1 were significantly increased. Furthermore, Hoechst 33258 staining and Aβ(1-40) ELISA results showed that DEX+Aβ(25-35) treatment induced hippocampus CA1 neuron apoptosis and increased the level of Aβ(1-40). The results suggest that the simultaneous effects of GCs and Aβ may have important roles in the etiopathogenesis of AD, and demonstrate that stressful life events and GC therapy may increase the toxicity of Aβ and have cumulative impacts on the course of AD development and progression.

Topics: Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; Analysis of Variance; Animals; Apoptosis; Arabidopsis Proteins; Caspase 3; Cytochromes c; Dexamethasone; Disease Models, Animal; Drug Synergism; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Glucocorticoids; Hippocampus; Intramolecular Transferases; Learning Disabilities; Male; Maze Learning; Memory Disorders; Microscopy, Electron, Scanning; Neurons; Peptide Fragments; Rats; Rats, Sprague-Dawley; Time Factors

2012