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Complement regulators C1 inhibitor and CD59 do not significantly inhibit complement activation in Alzheimer disease
K Yasojima1, E G McGeer, P L McGeer
1Department of Psychiatry, Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada.
Brain Research
|June 22, 1999
Summary
Complement activation in Alzheimer disease (AD) brains is not suppressed by regulators C1-inhibitor (C1-inh) and CD59. These regulators showed minimal increase, unlike complement components, suggesting ineffective suppression in AD and heart attack.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Activated complement proteins are found in Alzheimer disease (AD) lesions.
- The classical complement pathway requires overcoming regulators like C1-inhibitor (C1-inh) and CD59 for activation.
Purpose of the Study:
- To investigate the mRNA and protein levels of C1-inh and CD59 in AD brains compared to control brains.
- To compare the levels of these regulators with complement components in AD.
Main Methods:
- Reverse transcriptase-polymerase chain reaction (RT-PCR) to assess mRNA levels.
- Western blotting to assess protein levels.
- Analysis of brain tissue from AD patients and controls.
Main Results:
- C1-inh and CD59 were only slightly upregulated in severely affected AD brain regions.
- Ratios of AD to control mRNA for C1-inh and CD59 were significantly lower than for complement components (e.g., C9).
- Peripheral organ expression of C1-inh and CD59 showed minimal upregulation in infarcted heart tissue compared to complement components.
Conclusions:
- Endogenous regulators C1-inh and CD59 do not effectively suppress complement activation in Alzheimer disease.
- The upregulation of complement in AD and myocardial infarction is not adequately controlled by these inhibitors.