C5L2: A Decoy Complement Receptor With Anti-Inflammatory Properties in Alzheimer’s Disease
Susan O. McGuire, Ph.D.
Loyola University Medical Center
Maywood, Illinois
2005 New Investigator Research Grant
Though our immune system protects us from foreign organisms, it can, in some circumstances, cause inflammation and even death of our own cells and organs. Because the brains of people with Alzheimer’s disease show signs of chronic inflammation, it is widely believed that the immune system may be contributing to disease progression.
Susan O. McGuire, Ph.D., and colleagues will examine the relationship between Alzheimer’s disease and proteins of the immune system that contribute to inflammation. The researchers hypothesize that, as the disease progresses, there may be a shift of emphasis in the immune system, such that it begins producing more toxic proteins and fewer protective ones. This shift could be brought on by loss of a chemical called noradrenalin, which is made in a region of the brain that is damaged early in the disease. Previously, the researchers discovered that noradrenalin stimulates production of an immune system protein called C5L2, which may sequester toxic proteins and therefore protect cells in the brain.
To test these theories, the researchers will measure the amount of C5L2 and other immune system proteins in brain samples taken from people who had Alzheimer’s disease. They will also carry out experiments in cultured cells and in laboratory rats to determine if C5L2 does indeed protect nerve cells. This work may identify factors that could contribute to or relieve brain inflammation that occurs during progression of the disease.





