Nearly 500 scientists, advocates and others interested in health and aging gathered in Natcher Conference Center recently for “Advances in Geroscience: Impact on Health-span and Chronic Disease.”
NIA’s Dr. Felipe Sierra, of the geroscience interest group, speaks at the recent summit.
The meeting’s focus on “geroscience,” an integrated approach to the study of the diseases and disability associated with growing older, offered participants an opportunity to explore the interplay between chronic disease and its biggest risk factor—aging—in the hope of eventually opening new avenues for prevention and treatment.
NIH director Dr. Francis Collins welcomed participants, noting that geroscience represents the convergence of diverse areas of medical and scientific research on aging and disease. Increasingly, he said, a more careful study of the process of aging is allowing scientists to propose that risk factors for disease, including aging, need to be considered together rather than in isolation. This applies to most major chronic diseases including cardiovascular disease, cancer, Alzheimer’s and many others.
As an example, Collins mentioned his own research interest in Hutchinson-Gilford progeria, a rare genetic disease that causes premature aging in young children. He pointed out that the immunosuppressant rapamycin, which has been found to minimize some of the effects of progeria, also has been shown in other aging-related research to extend the lifespan of mice by mimicking the effects of calorie restriction.
Geroscience, he said, is “a field in wonderful ferment…that has the potential of showing a path toward longevity.”
The summit was developed by a relatively new organization—the trans-NIH geroscience interest group, or GSIG. With some 20 institutes and centers participating, the group was founded by program scientists from NIA and other institutes to find ways to collaborate and coordinate efforts.
The conference brought together 50 investigators from several disciplines to examine how the biology of aging drives chronic disease. Following Collins’ remarks, Dr. Christopher Murray, professor of global health at the University of Washington; Dr. Brian Kennedy, president and CEO of the Buck Institute for Research on Aging; and Dr. Linda Fried, dean of the Mailman School of Public Health at Columbia University, presented talks.
Murray discussed the Global Burden of Disease, Injuries and Risk Factors Study, a systematic effort to assess and compare the magnitude of “health loss” worldwide. Health loss is a comparison of reported health and death rates in a population against some ideal, which in this case is full health with a life expectancy of 86 years. The study measures more than 1,000 clinical outcomes, including the prevalence of—and mortality due to—many chronic diseases, lifespan and years lived with disability.
Murray noted that the study, with its vast online database of results, helps identify patterns of disease and disability. It offers geroscientists a valuable source of data about changes in risk factors such as high blood pressure and obesity. Drilling down into these data could help scientists and others target interventions to improve health and guide public health policy and spending.
NIH director Dr. Francis Collins discusses his research on progeria.
Photos: Bill Branson
With the global population over age 65 projected to rise to 2 billion by 2050, Kennedy said, studying the molecular causes of aging could one day help humans live in better health. “The events that are driving aging are the events that are driving disease,” he said, citing inflammation, stress and the adaptation to stress that occur during the aging process over time, changes in epigenetics, changes in metabolism and the onset of macromolecular damage with age. “It is my hope that thinking about aging processes and using this as an opportunity to look at diseases of aging from a new perspective may lead to new therapeutic approaches to treating them.”
Fried, a clinician-researcher, addressed frailty and aging, asking about possible biological underpinnings. Frailty is a syndrome of shrinking, slowing and weakness with low activity and low energy that increases with age and predicts disability and mortality. It also is linked to a range of chronic diseases including cardiovascular disease, late-life depression and inflammatory diseases. “There is mounting evidence that the biological changes of aging are the drivers of frailty,” Fried said, noting that changes at the molecular and genetic levels leading to frailty may also be involved in the development of disease.
Seven scientific sessions addressed topics in aging and chronic disease. At one panel, researchers discussed how low-grade, persistent inflammation associated with aging—a condition panel co-chair Dr. Claudio Franceschi of the Università di Bologna calls “inflammaging”—differs from the protective immune response and repair mechanism and contributes to risk for chronic disease. Another panel on epigenetics discussed several mechanisms by which it regulates genes at the chromatin level and how epigenetic changes contribute to aging and chronic disease. All the sessions explored such commonalities in aging and disease, looking at what is known and what would be beneficial to find out.
At the end of the conference, NIA director Dr. Richard Hodes said he hoped the meeting would encourage further conversations about commonalities of the mechanisms of aging and their impact on disease. NIH is committed to fostering this approach to research, he said, encouraging the audience “to maintain contact with those of us at NIA and all the institutes that have been collaborating here to make sure we make a go of this…we’re certainly not going to be bashful about following scientific imperative.”