NIH hosts national research summit on link between aging processes, chronic disease
Media invited to Oct 30-31 event
WHAT: “Advances in Geroscience: Impact on Healthspan and Chronic Disease” is a scientific summit bringing together 50 renowned investigators to examine how the basic biology of aging drives chronic disease. With aging known to be the single biggest risk factor for the development of non-genetic, chronic diseases, a better understanding of this interplay should open up new avenues for prevention and cures. The meeting reflects the emergence of the concept of “geroscience,” which features an integrated approach to the study of diseases and disability associated with growing older. Follow the meeting on Twitter using #AgingSummit.
WHO: Keynote speakers include: Francis S. Collins, M.D., Ph.D., Director, National Institutes of Health (NIH); Brian Kennedy, Ph.D., President and CEO, Buck Institute for Age Research; Linda Fried, Ph.D., Dean, Mailman School of Public Health, Columbia University; Christopher Murray, M.D., D.Phil., Professor of Global Health, University of Washington
WHEN: Wednesday and Thursday, October 30–31, 2013, 8:00 a.m. – 5:00 p.m.
WHERE: Natcher Conference Center at NIH, 9000 Rockville Pike, Bethesda, MD, 20892
In addition to a plenary session with the keynote speakers, the summit features seven scientific sessions covering inflammation, adaptation to stress, epigenetics, metabolism, macromolecular damage, proteostasis, and stem cells and regeneration. (A brief summary of these sessions appears at the end of this note.)
The summit was organized by the trans-NIH GeroScience Interest Group (GSIG) and co-sponsored with the Alliance for Aging Research and The Gerontological Society of America, with additional private sector support through the Foundation for the National Institutes of Health (FNIH). The GSIG was formed to focus on the relationships between aging and age-related diseases and disability and is among the newest trans-NIH interest groups. Additional information and the agenda are available at: www.geron.org/gerosciencesummit.
Media are invited to attend the meeting, which will be held on the NIH campus in Bethesda, MD. Please contact the communications office at the NIH’s National Institute on Aging at email@example.com or 301-496-1752 if you plan to attend.
Aging is generally characterized by a decline in physical and cognitive abilities and increased susceptibility to disease. Geroscience looks at mechanisms by which the basic biology of aging drives chronic diseases prevalent among the older population. These studies may lead to identifying critical features for future interventions. The Summit focuses on seven broad areas of research, representing multiple interactions between aging and disease variables:
Inflammation. Chronic inflammation plays a featured role in aging and many age-related diseases. It is perhaps the most significant risk factor for morbidity and mortality in older people. Researchers will address questions about whether inflammation is a cause or consequence (or both) of disease and the extent to which some inflammation might be beneficial.
Adaptation to Stress. The enhanced ability to adapt and adequately respond to stress is often observed in long-lived organisms. Mild stress appears to be protective and the ability to properly respond to chronic stress is necessary to promote healthy aging. The point at which mild stress becomes damaging, and whether the ability to deal with stress can be harnessed to decrease disease susceptibility will be discussed.
Epigenetics. Aging and susceptibility to disease are driven by both genetic and non-genetic (environmental) factors. Epigenetics is where these factors intersect—researchers believe that epigenetic alterations in the genome are affected by the environment. The epigenome of older people therefore reflects a lifetime of interactions with the environment. This concept will be explored along with how epigenetics presents new opportunities for intervention.
Metabolism. The way the body produces and uses energy is believed to be at the core of the biology of aging. Both dietary restriction and the drug rapamycin extend lifespan in mice by interfering with nutrient-sensing and cellular metabolism. Researchers will discuss evidence suggesting that improving metabolic efficiency might be effective to combat age-related disease processes.
Macromolecular Damage. Aging is accompanied by increased damage to proteins, lipids (fats), and DNA. To what extent this damage relates to aging and susceptibility to disease is unknown. Researchers are also reevaluating the role of free radicals (a byproduct of metabolic activity). Previously thought to drive aging, free radicals may actually be a signal alerting the body of potential danger.
Proteostasis. Maintaining the quality of proteins under varying conditions is essential to preserve cell function and adapt to changing environments. Proteostasis prevents the accumulation of misfolded proteins and consequent health problems, but efficiency decreases with age. Improved understanding of proteostasis may lead to new aging and disease therapies. The session will focus on questions about proteostasis that relate to health span extension.
Adult Stem Cells and Regeneration. Stem cells are a potential cure for many age-related degenerative diseases. Recent work has focused on characterizing adult stem cells and their activities during aging. They are often present in older mice, but with reduced or altered function. Questions regarding stem cell interactions with their environment and ways to preserve stem cell quality during aging will be discussed.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
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