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Inflammation, the complement system and the diseases of aging.
Edith G McGeer1, Andis Klegeris, Patrick L McGeer
1Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada.
Neurobiology of Aging
|October 4, 2005
Summary
Inflammation contributes to neuron destruction in aging neurodegenerative diseases like Alzheimer's and Parkinson's. Anti-inflammatory agents may offer broad therapeutic benefits for these conditions.
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Neuroinflammation is a key feature of age-related neurodegenerative diseases.
- Evidence suggests a link between activated glial cells (microglia and astrocytes) and neuronal damage.
- Observational studies show reduced incidence of Alzheimer's disease, Parkinson's disease, and age-related macular degeneration in long-term anti-inflammatory drug users.
Purpose of the Study:
- To investigate the role of inflammation in the pathogenesis of neurodegenerative diseases.
- To explore the potential of anti-inflammatory strategies for treating these conditions.
Main Methods:
- Review of neuropathological findings in lesioned brain areas.
- Analysis of epidemiological data on long-term users of anti-inflammatory agents.
- Identification of key inflammatory mediators involved in neuronal damage.
Main Results:
- Activated microglia and astrocytes are present in lesioned areas of neurodegenerative diseases.
- Long-term use of anti-inflammatory agents is associated with a lower prevalence of Alzheimer's disease, Parkinson's disease, and age-related macular degeneration.
- The membrane attack complex (MAC) and oxygen-free radicals are identified as locally produced autodestructive molecules.
Conclusions:
- Inflammation appears to be an autodestructive process contributing to neuronal loss in aging.
- Targeting inflammation with appropriate agents could offer a broad therapeutic approach for various neurodegenerative diseases of aging.