Harvard symposium highlights antiaging therapies and shows the maturation of a field.
Pat McCaffrey
Everybody’s doing it: aging, that is. And, it seems everybody’s getting into aging research as well, judging by the number of scientists that gathered Monday for the first annual Harvard/Paul F. Glenn Symposium on Aging.
Held at Harvard Medical School and hosted by a year-old privately funded aging lab at Harvard, the one-day conference highlighted just how far this once-shunned field has come, and how fast it’s moving.
Boston is ground zero for the discovery of the genetic regulation of aging. Keynote speaker and MIT professor Leonard Guarente was first to discover the longevity gene SIR2 in yeast in 1991. With his work, the idea that aging is a regulated genetic program took hold.
But the field was still very young. In the second keynote of the conference, Cynthia Kenyon of the University of California, San Francisco, talked about how in the early 1990s she had trouble enticing graduate students to work on aging in worms.
Then her lab identified a single genetic mutation that doubled the worms’ life span. After that, she had no problem attracting interested young researchers.
Both SIR2 and the aging gene that Kenyon discovered have counterparts in higher organisms, and their discoveries triggered a massive acceleration in human aging research.
These days, established scientists who haven’t done much research on aging find themselves moving into the field. That’s because the goal of aging research has evolved beyond simply maximizing life span to increasing the number of healthy years a person can enjoy. That means tackling the diseases of aging. This expanded focus is attracting people doing research on diseases from diabetes to Alzheimer’s disease and cancer.
This trend was obvious at the aging symposium. The event’s host, the Glenn Laboratories for the Biological Mechanisms of Aging at Harvard Medical School, was established last year with $5 million from Paul F. Glenn, a charismatic California businessman with a long-standing interest in aging research.
A key aim of the lab is to bring researchers working on chronic diseases into the fold of aging studies. “Right here we had the leaders in the field of aging,” says David Sinclair, a Harvard Medical School professor and director of the lab. “They just didn’t know it until now.”
For example, the lab’s codirector, Bruce Yankner, worked on Alzheimer’s disease for years until he became frustrated by how little he knew about brain aging, which is the number-one risk factor for dementia.
Now he is studying the brains of healthy centenarians to learn about the natural defense mechanisms that protect the brain in long-lived humans. Understanding and finding ways to alter these pathways could protect the elderly against neurodegenerative diseases.
Signal transduction specialist Lewis Cantley of Harvard is also a newcomer to aging research. He discovered pathways involved in diabetes and cancer that are connected to the SIR2-related pathways.
Sinclair ended the day with a talk about his latest results on extending the life span of mice. In 2003, he found a plant product abundant in red wine, resveratrol, that activates SIR2-related proteins. Later, he showed how this process extended the life of lower organisms. It appears that resveratrol may have the same effect in mice, too.
According to unpublished data, mice that were fed a high-fat, high-calorie “western diet” that included resveratrol had a similar metabolism (such as insulin and blood glucose levels) as those fed a more healthy diet. By the ripe old age of two, many of the mice on the “western diet” that did not include resveratrol were already dead, while those receiving it thrived.
Sinclair suggests that resveratrol may be a starting point to generate better drug candidates. So while the aging field has gained legitimacy over the years and expanded in scope, it still retains one of its original goals: finding the elusive antiaging pill.
Pat McCaffrey is a freelance writer in Auburndale, Massachusetts.