More than five million Americans have Alzheimer’s, a mind-robbing disease without a cure. And that number is expected to triple as baby boomers age.
This week researchers meeting in Vancouver will learn whether an experimental treatment appears to be working. It’s one of several drugs scientists are testing in the hopes of reducing beta-amyloid peptide, a sticky protein which gums up the brain.
In this Health Checkup, Shelley Kofler talks with Alzheimer’s expert Dr. Mary Quiceno of UT Southwestern Medical Center. She explains why targeting beta-amyloid may lead to a treatment or cure for Alzheimer’s.
Quiceno: Beta amyloid is what we find in the brain of people who have Alzheimer’s disease. It seems to be as we get older, either people have a genetic problem with amyloid and they make too much, or don’t process it efficiently. So instead of getting rid of it like we normally should, it starts to build up in the brain.
Once it’s there, unfortunately the first place it usually goes is that part of the brain that has to do with memory and learning and it disrupts the function of the cells. The cells don’t like it to be there and it kills them.
Kofler: We’ve heard recently about numerous research projects that are targeting beta amyloid, trying to prevent it from becoming excessive. How close are we to a breakthrough?
Quiceno: This week, there is a very important international meeting sponsored by the Alzheimer’s Association in Vancouver, and we’re going to have some important announcements about the drugs that are in trial right now, targeting amyloid, and if they’re working or not. I’m very optimistic about the future of Alzheimer’s disease treatment and that is because many researchers here at UT Southwestern and around the world are looking at therapies that we’re going to use earlier and earlier.
We know that, from a recent study from Washington University, that amyloid starts to become abnormal many decades before the onset of the disease. So we know we have to start going back, you know, maybe at the point when they first start developing abnormal amyloid. So it could be many decades before they develop memory loss where we have time to intervene and influence the amyloid deposits in the brain.
At UT Southwestern, we’re just getting started to be able to provide pet scans, so we can image amyloid. We can look at that in people who don’t yet have dementia, and so we can find them early, and now the second part of that is giving the treatments.
I work very closely with Dr. Roger Rosenberg, an internationally known researcher, and he’s developing a vaccine against Alzheimer’s disease. And that could be something we could give people regardless of what their amyloid load level is.
Kofler: If this research proves really promising, how long will it be before we can apply that knowledge to something that’s practical, on the ground, affecting patients?
Quiceno: Not soon enough. But I think that within the next decade, decade and a half, I really think we’re going to be at that point where we have the therapy to offer people who are just very mildly symptomatic and we may even be on the cusp of some sort of preventative.
Kofler: So in the meantime, for those of us with family members who already have Alzheimer’s, what kind of hope is there for a good life?
Quiceno: I’m very optimistic about that. I think that we’re finding ways not just with drugs, that take a long time to develop, but with other things that people can do now. We know that exercise can directly affect growth of brain cells, and improve memory and cognition. Cognitive training or building of cognitive reserve. We know that protects you from dementia in later life. Diet plays an important role as well.
If my patients and subjects in research and counsel, and for their family members, because they always want to know, too, “What can I do to prevent this?” I always talk about, those are things that you can do now, but you really have to think about those as important, and just as important as taking a pill: keeping your brain and your heart healthy.
