Thesis #36 – Experimental populations which have evolved different time-points for the cessation of aging can be used to uncover the biological foundations that determine the timing of the cessation of aging.
During the 1980s and 1990s, my laboratory devoted a significant proportion of its efforts to working on the biology of fly populations that had slowed aging. Many of these studies are gathered together in the book Methuselah Flies, which came out in 2004. We deliberately left our research on the cessation of aging out of that book. So what the book reflects is our attempts to study the kind of physiological changes that are involved in making a fruit fly age at slower rate. One of the surprising things about that research was how basic or elementary the changes involved were, from the standpoint of physiological subtlety. The issues that are important to fruit fly aging, as far as the flies themselves are concerned, involve whole-organism attributes like the allocation of fats between survival and reproduction, the extent to which flies hang on to their water reserves, and so on.
Similar studies can be made of flies that have different time-points at which aging stops. One of my senior graduate students as of this writing, Parvin Shahrestani, is now studying the whole-organism physiology of both aging and the cessation of aging in fruit flies that have very different ages for the cessation of aging. We don’t yet know what her results are going to look like, but the experimental project itself is relatively straightforward.
There is no reason why we cannot figure out the physiology that lies behind such shifts in aging and its cessation. All my laboratory lacks is the resources to make the study of this question more intensive than we have managed to this point, the natural result of getting too far ahead of our colleagues on the panels of granting agencies.
In addition to Parvin Shahrestani’s whole-organism research, we have an early view of the genomics that underlie wholesale shifts in patterns of aging and its cessation. This was the work of my graduate student, Molly Burke, published in the journal Nature in September 2010. Her work shows that many genes may be involved in shifting patterns of aging and its cessation. Thus, at the molecular level, the foundations of transforming aging and its cessation are quite complex.
It will take some time for the biological research community to establish the specific genetic and physiological mechanisms that can be used to slow aging and to stop it. Fortunately, as we will now discuss, we have recently discovered some exciting short-cuts that might provide us with partial solutions. These can be thought of initial down payments toward the detailed genome-wide, cell-wide, and organism-wide findings with which we will eventually fully decode the complex networks which underlie aging. But I think that you will find them promising nonetheless, as you work through the rest of the 55. These short-cuts involve environmental manipulation. Thus the 55 now turn to the biology that underlies not the evolution of aging or the evolution of its cessation, but instead the biology that underlies the effects of environmental change on aging and its cessation.