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Complement activation in very early Alzheimer disease.
H Zanjani1, C E Finch, C Kemper
1Andrus Gerontology Center and Department of Biological Science, University of Southern California Los Angeles, California, USA.
Alzheimer Disease and Associated Disorders
|June 9, 2005
Summary
The complement system (C) is activated in early Alzheimer
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- The complement system plays a role in neuroinflammation.
- Its involvement in early Alzheimer disease (AD) pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the activation of the complement system in early-stage Alzheimer disease (AD) and non-demented aging.
- To determine the stage-specific deposition of complement fragments and regulators in AD brains.
Main Methods:
- Immunohistochemistry was used to detect complement fragments (C1q, C3, C4, C5b-9) and regulators (CD59, CR1, DAF, MCP) in brain tissue.
- Subjects were assessed using the Clinical Dementia Rating (CDR) scale.
Main Results:
- Complement activation (C3, C4) was observed in all brains with amyloid deposits, including non-demented individuals and preclinical AD.
- Complement fragment deposition increased with plaque density in AD.
- Early complement components (C1q, C5b-9) were detected in very mild AD, and consistently in severe AD.
- Complement regulators were notably absent from plaques and tangles, indicating incomplete control.
Conclusions:
- Complement system activation is an early event in Alzheimer disease pathogenesis, occurring even before clinical symptoms.
- The deposition of complement fragments correlates with AD progression and amyloid pathology.
- Incomplete regulation of complement activation in AD suggests a potential therapeutic target.