Abstract
It has been demonstrated that the onset and progression of Alzheimers disease (AD) are associated with inflammatory disorders in the brain. Although the interactions of inflammatory cytokines with neurotrophins have been reported in vitro, the balance change between inflammatory cytokines and neurotrophic factors (NTFs), such as nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF), due to amyloid β (Aβ) chronic administration in vivo is still unclear. The hypothesis of the present study was that the accumulation of Aβ activated glial cells to produce inflammatory mediators and NTFs to maintain the neurons survival, however the failure of crosstalk between NTFs and inflammatory cytokines might occur in the brain and the NTFs expressions would decrease after Aβ chronic treatment, which, therefore, would contribute to the neuronal death and memory impairments. Thus, the present study measured the learning and memory behavior, glial cells activities, cytokines (IL-1α, IL-1β and TNF-α) concentrations and NTFs (NGF, BDNF and GDNF) gene and protein levels in rats after i.c.v injection of Aβ25-35 for 14 days. The results showed that Aβ25-35-treated animals exhibited failure of balance between inflammatory cytokines and NTFs system (increased cytokines levels, decreased NGF protein expression and reduced NTFs gene transcriptions), which might contribute to the cognitive impairments. The findings from this study provide valuable evidence that correct regulation of the crosstalk between inflammatory cytokines and NTFs could be a direction for AD therapy in the future.
Keywords: Alzheimer's disease (AD), neurotrophic factors (NTFs), inflammatory cytokines, microglia, astrocytes, amyloid beta, amyloid plaques, antigen, alpha, interleukin, neuron, proliferation, 3 cytokines
Current Alzheimer Research
Title: The Mechanism of Memory Impairment Induced by Aβ Chronic Administration Involves Imbalance between Cytokines and Neurotrophins in the Rat Hippocampus
Volume: 8 Issue: 4
Author(s): C. Ji, C. Song and P. Zuo
Affiliation:
Keywords: Alzheimer's disease (AD), neurotrophic factors (NTFs), inflammatory cytokines, microglia, astrocytes, amyloid beta, amyloid plaques, antigen, alpha, interleukin, neuron, proliferation, 3 cytokines
Abstract: It has been demonstrated that the onset and progression of Alzheimers disease (AD) are associated with inflammatory disorders in the brain. Although the interactions of inflammatory cytokines with neurotrophins have been reported in vitro, the balance change between inflammatory cytokines and neurotrophic factors (NTFs), such as nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF), due to amyloid β (Aβ) chronic administration in vivo is still unclear. The hypothesis of the present study was that the accumulation of Aβ activated glial cells to produce inflammatory mediators and NTFs to maintain the neurons survival, however the failure of crosstalk between NTFs and inflammatory cytokines might occur in the brain and the NTFs expressions would decrease after Aβ chronic treatment, which, therefore, would contribute to the neuronal death and memory impairments. Thus, the present study measured the learning and memory behavior, glial cells activities, cytokines (IL-1α, IL-1β and TNF-α) concentrations and NTFs (NGF, BDNF and GDNF) gene and protein levels in rats after i.c.v injection of Aβ25-35 for 14 days. The results showed that Aβ25-35-treated animals exhibited failure of balance between inflammatory cytokines and NTFs system (increased cytokines levels, decreased NGF protein expression and reduced NTFs gene transcriptions), which might contribute to the cognitive impairments. The findings from this study provide valuable evidence that correct regulation of the crosstalk between inflammatory cytokines and NTFs could be a direction for AD therapy in the future.
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Ji C., Song C. and Zuo P., The Mechanism of Memory Impairment Induced by Aβ Chronic Administration Involves Imbalance between Cytokines and Neurotrophins in the Rat Hippocampus, Current Alzheimer Research 2011; 8 (4) . https://dx.doi.org/10.2174/156720511795745366
DOI https://dx.doi.org/10.2174/156720511795745366 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
Call for Papers in Thematic Issues
New Advances in the Prevention, Diagnosis, Treatment, and Rehabilitation of Alzheimer's Disease
Aims and Scope: Introduction: Alzheimer's disease (AD) poses a significant global health challenge, with an increasing prevalence that demands concerted efforts to advance our understanding and strategies for prevention, diagnosis, treatment, and rehabilitation. This thematic issue aims to bring together cutting-edge research and innovative approaches from multidisciplinary perspectives to address ...read more
Current updates on the Role of Neuroinflammation in Neurodegenerative Disorders
Neuroinflammation is an invariable hallmark of chronic and acute neurodegenerative disorders and has long been considered a potential drug target for Alzheimer?s disease (AD) and dementia. Significant evidence of inflammatory processes as a feature of AD is provided by the presence of inflammatory markers in plasma, CSF and postmortem brain ...read more
Deep Learning for Advancing Alzheimer's Disease Research
Alzheimer's disease (AD) poses a significant global health challenge, with an increasing number of individuals affected yearly. Deep learning, a subfield of artificial intelligence, has shown immense potential in various domains, including healthcare. This thematic issue of Current Alzheimer Research explores the application of deep learning techniques in advancing our ...read more
Diagnostic and therapeutic biomarkers of dementia
Dementia affects 18 million people worldwide. Dementia is a syndrome of symptoms caused by brain disease, usually chronic or progressive, clinically characterized by multiple impairments of higher cortical functions such as memory, thinking, orientation, and learning. In addition, in the course of dementia, cognitive deficits are observed, which often hinder ...read more
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