When the Buck Institute for Research on Aging opened in 1999 in Novato, Calif.,
“biogerontology” was a little-known subset of of gerontology. It looked completely different than it does today.
“At the time the Buck started, there was nothing like it,” says Brian Kennedy, Ph.D., its president & CEO. “It was a difficult battle trying to get aging research noticed.”
But then aging researchers at the Buck and elsewhere began to solve the mysteries of why our bodies age.
“It used to be that aging was considered a fixed process. But then in the mid-90s we started finding genetic mutations that extended lifespan,” says Kennedy. “That was an important step. It was possible to modify aging.”
Over the next 20 years, more discoveries were made, spurred in large part by the sequencing of the human genome in 2003.
Fast forward to 2015. Biogerontology has morphed into geroscience – a discipline that has moved into the mainstream of science and is even mentioned on Capitol Hill. Researchers working in the trenches have begun to figure out why our bodies get older. And they are really focused on aging as the common cause of a panoply of chronic conditions, including Alzheimer’s, Parkinson’s, cancer, arthritis, and cardiovascular disease, among others.
The Buck Institute has become one of the main centers for aging research.
“Our purpose at the Buck is to extend human healthspan. We need to find ways to make people live healthier, longer, and that is what we are doing,” he explains.
The Buck has a team of 22 faculty in independent labs working to uncover the mysteries of why we age. Half of them focus on finding the pathways that govern why we age and the other half on specific diseases of aging.
A current project Kennedy expresses excitement about revolves around the testing of drug interventions in mice. The focus is less on the drugs’ impact on the lifespan of mice, but rather on how the drugs affect function as the mice age. Kennedy says these trials will hopefully bridge the gap to the next step: the testing of interventions to slow aging in humans.
That is that ultimate goal that scientists like Kennedy seek: to slow aging in order to prevent disease and promote good health so that growing old no longer means growing ill. We are getting close, but we aren’t quite there yet, he adds.
“We are getting good at modifying aging, but we are still trying to figure out what causes aging. It isn’t one thing,” he notes. “We need to figure out how to connect the dots.”
The good news is that there are many scientists at work on this challenge. They are also collaborating like never before. Kennedy was recently part of a group of experts who released a strategy focused on seven critical “pillars of aging.” This was inspired by a 2013 conference of the National Institute of Health’s Geroscience Interest Group.
“I think there are people in the aging field who are putting a concerted effort into getting the word out. There are more of us out there,” says Kennedy.
This is especially important as our population ages. With longer lives and more people over the age of 65 every day, the idea of extension of healthy aging has become an issue of national importance.
And the future of geroscience?
Kennedy thinks we are making progress. The research is starting to connect those dots he mentioned.
The research his institute conducts. The work going on at NIH. The almost-monthly discoveries by experts across the globe.
Kennedy says this is a historic opportunity for science:
“We are going to look back on this century. Will it be a time when we didn’t address the problem of chronic disease and all of the consequences that went with it? Or did we decide to target chronic diseases of aging to ensure these people were healthy instead? I hope we chose healthspan.”