Dr. Sidney Strickland is a recognized leader in the study of vascular factors and their effects on Alzheimer’s disease. A colleague of Dr. Paul Greengard, Director of the Fisher Center for Alzheimer’s Research laboratory at The Rockefeller University, Dr. Strickland is head of the Laboratory of Neurobiology and Genetics and dean of graduate and postgraduate studies there.
Dr. Strickland and his team study the molecular mechanisms of nerve cell death and regeneration, with a special focus on Alzheimer's disease. Preserving Your Memory spoke with Dr. Strickland about his research work.
PYM: Why is inflammation such an important consideration in brain health?
Dr. Sidney Strickland: Inflammation is a good process in most circumstances. It’s what the body uses to fight infection and tissue damage. But if it’s chronic and goes unchecked, it can be very deleterious. What we’ve uncovered is a process in Alzheimer’s disease that can lead to chronic inflammation, which can kill neurons and cause damage in the brain.
PYM: How do the beta-amyloid peptide and fibrinogen interact with each other?
SS: They have a physical interaction. Fibrinogen is the major protein component of blood clots. When the Alzheimer’s disease beta-amyloid peptide binds to fibrinogen, the clot that is formed is abnormal and hard to degrade. This persistent clot can promote the chronic inflammation that I mentioned earlier.
PYM: How does the beta-amyloid peptide affect the brain?
SS: It’s not exactly known how it affects the brain. That’s what everyone is looking for. Our results show that the beta-amyloid peptide can interact with clotting components and lead to persistent blood clots. In addition to persistent clots leading to chronic inflammation, they can lead to less blood flow to critical areas of the brain. If you don’t have blood flow to those areas, the tissues die. So persistent clots can create less blood flow and inflammation, and both those processes can end up killing cells.
PYM: What are the prospects for new Alzheimer’s disease treatments or therapies coming out of your research?
SS: This is one exciting aspect for us because there are new therapeutic strategies that evolve from our study. We don’t think there will be just one therapy for Alzheimer’s disease; there will probably be many therapies that attack various aspects of the disease. So if we could block the interaction of the beta-amyloid peptide with fibrinogen, it would prevent the formation of persistent clots, but it wouldn’t affect normal clotting. In this case, a person would not have bleeding tendencies, but would not have the formation of the beta-amyloid peptide-induced abnormal clots that can cause damage. We predict in this case that there would be beneficial effects on the cognitive dysfunction that characterizes Alzheimer’s disease.