It’s an uncomfortable truth that aging is the single biggest risk factor for many chronic diseases. It’s also completely out of our control. (The alternative is, well, not so fun to contemplate.) But although we all think we’d like to live longer, longevity in and of itself is not necessarily a good thing. Living longer rapidly loses its appeal if you’re too sick or feeble to really enjoy your extra “golden” years.
But researchers from many scientific disciplines are now working to understand how and why our bodies tend to break down as time passes. The Trans-NIH Geroscience Interest Group (a group of researchers from numerous NIH institutes) interested in aging held a summit in 2013 to explore mechanisms of aging and identify common themes that could serve as research targets. The thought is that understanding, and slowing, aging may be an efficient way to tackle many chronic diseases simultaneously.
Now the group, which includes Stanford geneticist Anne Brunet, PhD; neurologist Tony Wyss-Coray, PhD; and Thomas Rando, MD, PhD, has released the conclusions of the summit and outlined a plan for the work that lies ahead. (Rando is the director of the Glenn Center for the Biology of Aging at Stanford.) Many of the findings focus on a concept called “healthspan,” which designates the portion of a person’s lifespan in which he or she is relatively healthy and fully functional. From the Cell article:
While life expectancy continues to rise, healthspan is not keeping pace because current disease treatment often decreases mortality without preventing or reversing the decline in overall health. Elders are sick longer, often coping with multiple chronic diseases simultaneously. Thus, there is an urgent need to extend healthspan.
The researchers identified seven intertwined “pillars of aging” for targeted research, including adaptation to stress, stem cells and regeneration, metabolism, macromolecular damage, inflammation, epigenetics and a concept called proteostasis, which describes the intricate dance in which proteins are made, transported and degraded within a cell. They suggest the creation of an Aging Research Initiative that works to merge the emerging field of geroscience with research on chronic disease and to search for therapeutic interventions that could extend both lifespan and healthspan.
The article is a fascinating summary of what’s likely to be the trajectory of aging research during the next decade, and it outlines specific research approaches to accomplish the goals. For example, they suggest paying closer attention to companion dogs as an animal model, since our favorite canine buddies share many aspects of our environment and (like humans) exhibit a bewildering array of genetic diversity.
The authors conclude:
The goal of slowing aging has fascinated humankind for millennia but has only recently acquired credibility. Recent findings that aging can be delayed in mammals raise the possibility of prolonging human healthspan. There is near consensus among aging researchers that this is possible, but only if resources are available to accomplish goals in areas ranging from basic biology to translational medicine. […]
Although understanding the unique features of any given disease is laudatory and is potentially of therapeutic value, approaches to understand a common cause, aging, will be uniquely important. If we can understand how aging enables disease, it may be possible (and even easier) to target this common component of disease. Targeting aging may allow early intervention and damage avoidance, maintaining vigor and activity while offsetting the economic burdens of a burgeoning aging population hampered by multiple chronic diseases.
Previously: Girls at high risk for developing depression show signs of stress and premature aging, Even old brains can stay healthy, says Stanford neurologist and The rechargeable brain: Blood plasma from young mice improves old mice’s memory and learning
Photo by Vincent van der Pas