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Neuroinflammatory changes increase the impact of stressors on neuronal function
Alessia Piazza1, Marina A Lynch
1Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland.
Biochemical Society Transactions
|January 16, 2009
Summary
Age-related neuroinflammation exacerbates responses to stressors in the brain. Targeting neuroinflammation may slow the progression of neurodegenerative diseases.
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Neuroinflammation is a common feature in neurodegenerative diseases and aging.
- Age is a significant risk factor for neurodegenerative diseases, potentially linked to age-related neuroinflammation.
- Microglial activation exacerbates responses to stressors in experimental models.
Purpose of the Study:
- To discuss the role of age-related neuroinflammation in neurodegenerative diseases.
- To present in vitro and in vivo data on the interaction between amyloid beta-peptide (Abeta) and lipopolysaccharide (LPS).
Main Methods:
- Review of existing research on neuroinflammation and aging.
- In vitro experiments exposing cells to Abeta and LPS.
- In vivo experiments examining inflammatory responses.
Main Results:
- Responses to Abeta are significantly increased in the presence of LPS.
- Experimental conditions with up-regulated microglial activation show exacerbated stress responses.
- Findings suggest a vulnerability associated with inflammation.
Conclusions:
- Neuroinflammation may not be the primary cause but can accelerate neurodegenerative disease progression.
- Treating neuroinflammation could be a therapeutic strategy to decelerate disease progression.
- Age-related neuroinflammation may contribute to the increased risk of neurodegenerative diseases.
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