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| Brian Kennedy |
Projections show that six out of 10 Baby Boomers will be living with one or more chronic conditions by 2030, and the Buck has dedicated its resources to extending healthspan, the healthy years of an individual’s life. The independent nonprofit organization, based in Novato, Calif., is the nation’s first freestanding U.S. institute devoted solely to basic research on aging and age-associated disease. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating conditions such as Alzheimer’s and Parkinson’s disease, cancer and stroke.
Q: What do we know now about aging that we didn’t know, say, 10 or 20 years ago?
A: You can look at it from different ways. From a mechanistic perspective, we know a lot more potential things that are happening in our body that are driving the aging process. But we still don’t know the relevant contributions of different things like mitochondrial dysfunction — all those things happen with aging but we still don’t know how each of them contributes to the diseases of aging and mortality.
We have made a tremendous amount of progress in two areas. One is in the discovery of modulating agents. I think that it is clear now that aging is not intractable. You can actually slow aging — in all the model organisms now, from simple things like yeast and worms to mice and rats. The second area is dietary restriction. Last year it was shown that dietary restrictions extended the lifespan of primates.
Q: What are some of the biggest misunderstandings when it comes to aging and age-related research?
A: One of the biggest concerns is that the FDA doesn’t consider aging a disease. Now, why is that? I think the main reason is that 100 percent of the population gets it. So it is kind of a semantic argument, but it’s a problem because if you don’t consider something a disease, you cannot conduct a clinical trial.
There’s a very small amount of money that gets spent by the federal government on aging research. It is tiny in proportion to cancer. The NIH spends about $5 billion a year on cancer, about $3.5 billion on heart and lung disease, $2 billion on diabetes. They spend a little over $1 billion on aging but half of that is on Alzheimer’s, which is what I consider money well spent but is not what I would call a basic aging property. What we are saying is that we are spending a lot of money on the effects of aging, but aging is one of the causes. If you want to do something effective, you try to fix the primary problem, not the effects. But at the same time, the budget is shrinking on a federal level and we have to find ways to raise the money we need to do this research.
Q: The Buck mission is to increase the healthy years of life. So, in other words, you aren’t looking to necessarily extend life but to improve healthspan? Or, simply, take the edge off getting old?
A: It has long been known that cancer, neurodegeneration like Alzheimer’s disease, diabetes – these things increase dramatically in prevalence as we get older. And what we’re learning is that aging is actually a cause of these diseases – it is one of the causes. If you slow aging, you’re going to get benefits across a wide spectrum of disease.
What we want to emphasize is that extending healthspan is the most important thing, but extending lifespan might come along with that. But if you just tell people that you want to extend lifespan then they think about their 85-year-old grandmother who is sick and they think, “I don’t want to live longer than 85 when I am sick.” Now, the truth is that none of the models that we study do that. What they do is they extend healthspan — they make animals live longer until they start to get sick.
Q: Is it true that by studying aging, we might, for instance find the cure for cancer?
A: I think that what we’re going to find is effective, preventative measures to avoid the onset of cancer. And that’s probably true for cardiovascular disease, too. Things that slow aging are really preventing the onset of disease, and it is not yet clear in some of those cases that if you waited until after somebody got sick and then gave them the drug, whether that would be beneficial or not. That is something that is being studied but it is unknown at this point. The great study last year with rapamycin, a FDA-approved drug given to mice at 600 days of age (equivalent to a 65-year-old human), demonstrated how mice lived 15 percent longer, and lived healthier. So, I think that if you had a drug you could give to somebody at age 60, and have that kind of effect, there would be a lot of excitement around it.
Q: Talk about some of your most recent research. How does, for example, a compound intended for liver preservation become one looked at for Huntington’s disease?
A: People are starting to really understand that a lot of these different diseases have related components. Even though the mechanism of the disease is different, the events that make you prone to getting the disease in the first place may be more similar. Aging is one of those things. So the idea now is that if you have a drug, especially one that is clinically approved for one disease, thinking about it on a broader spectrum level is a useful thing to do.
From an academic perspective, we are looking at the most effective route to take the basic understanding that we have about aging and translate that to effective therapies for diseases. And using things that we already know are safe is one route to go down that path.
CHI-Advancing California biomedical research and innovation
