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Alzheimer disease and neuroinflammation
P L McGeer1, E G McGeer, K Yasojima
1Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Journal of Neural Transmission. Supplementum
|August 29, 2000
Summary
Alzheimer disease (AD) brains show significantly increased inflammatory molecules and activated microglia. Complement inhibitors remained unchanged, suggesting inflammation drives neuronal death in AD.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer disease (AD) is linked to inflammation and activated microglia.
- Brain cells are primary producers of inflammatory components in AD.
Purpose of the Study:
- To quantify inflammatory markers and complement regulators in normal versus AD brain tissue.
- To assess the role of inflammation in AD pathogenesis.
Main Methods:
- Measured mRNA levels of complement proteins, complement regulators (CD59, C1 inhibitors), C-reactive protein (CRP), and microglial markers (HLA-DR, CD11b).
- Compared these levels between normal and AD brain samples.
Main Results:
- Marked upregulation of inflammatory mediator mRNAs in AD tissue.
- Complement inhibitor mRNAs showed minimal change in AD brains.
- Upregulation of CRP and CD11b in AD hippocampus was comparable to osteoarthritic joints.
Conclusions:
- Chronic inflammation is strongly implicated in neuronal death in Alzheimer disease.
- The balance between inflammatory mediators and inhibitors is disrupted in AD.