Okay. Back to Aging.

by Brad

Okay. It’s been a while, as I’ve been busy with writing NIH grants and papers, as well as traveling. So it's time to get back to one of the central points of this blog: what is aging? It turns out this is no more clear than trying to define yoga. When I joined the Buck Institute for Research on Aging some 11 years ago, I was surprised and a little chagrined to discover how unsettled and wide open this central question of aging biology was.

This was not my original field of study, but as a chemist and structural biologist working at a major teaching university, I saw a prime opportunity to make a career shift by joining the Buck Institute and using my skill to elucidate molecular mechanisms of aging. But I had no idea how many competing theories existed on this subject, ranging from rather oblique terms like ”antagonistic pleotrophy” to more familiar ones—at least to a chemist—like “entropy” and “free radical damage.” So the other day when there was some news coverage in the New York Times of a breakthrough in aging research (see NY Times article here), I saw this as a chance to tackle this subject. The article, titled “In Body’s Shield Against Cancer, a Culprit in Aging May Lurk,” came out of the Mayo Clinic and looked at the role of senescent cells in aging (see original research here).

When cells reach a point of pathological state, either through telomere shortening or some other aberration or damage, a sequence of events are put into place that either sends these cells into a cell death pathway, or into a state of senescence, a kind of limbo non-dividing state. One reason this occurs is to avoid the formation of a cancerous cell, which the organism obviously wants to avoid. Cells that become senescent were usually thought of as sequestered cells that no longer posed a problem to the organism, but were also no longer productive. However, what this new study showed is that these senescent cells appear to have more damaging effects on neighboring cells and tissues, possibly through a secreted inflammatory signal.

Manzanita by Brad Gibson

By constructing a mutant mouse strain where the researchers could target and kill these senescent cells without harming the healthy cells, researchers found that it had a significant beneficial effect on the health of the mice, and that they lived longer. There is a lot of follow-up work to be done to confirm these studies in “normal mice” as well as in humans. In any case, the data are highly intriguing. It is also worth pointing out that when asked whether this would cure aging, the scientists were much more cautious, as they clearly understood that this is probably only one of many mechanisms that are contributing to aging. Nonetheless, it is interesting to see how inflammation comes up repeatedly as a cause or at least a driver of many age-related disease, from Alzheimer’s disease to diabetes.

One question that I would like to get back to is: what can we do as individuals to influence this process? What are the conditions that lead to cellular senescence versus cell death, for example, and what are the physiological and environmental determinants that cause as a cell to enter this critical state in the first place? If we knew the answers to these questions and as well other questions of this type, we might be able to critically examine how we can influence are own rate of aging. This question is related but separate from how we can reduce and/or cope with various age-related losses and pathologies as they emerge. Both questions will be critical to answer to reach an understanding on the practice of healthy aging.  How yoga might be a part of that practice is what we are trying to address here….