Engineering is in essence the business of producing good, workable solutions in absence of complete knowledge. The Romans could construct excellent bridges with a tiny fraction of the knowledge of materials science, mathematics, and modeling possessed by today's architects. Medical technologies today are in much the same position: we might know about as much of the fine details of biology as the Romans did of the deeper sciences underlying architecture. A vast scope of discovery and cataloging is yet to be accomplished in the life sciences. Yet we can still produce good therapies well in advance of a full understanding of human biochemistry.
Pure science as practiced today is the polar opposite of engineering. The goal is to produce complete understanding, and only then hand over that knowledge to those who will apply it to produce technologies. This is an ideal rather than the reality, of course: at some point in the development process there are always those who will make the last leap to clinical application because it is more cost effective to take a chance than to grind to the very end of the research process. The last stages of medical research are ever a compromise between the ethic of science, full understanding first, and the ethic of engineering, let's just get it done when there's a reasonable chance of success. Building proposed therapies and trying them out is sometimes the best path forward for both learning and application of knowledge.
In aging research the archetype of the engineering approach is the SENS program, scientific projects aimed at moving as rapidly as possible towards practical rejuvenation therapies. The SENS vision for development is explicitly a way to use our present knowledge of forms of cellular and tissue damage that cause aging in order to work around our present lack of knowledge regarding how exactly metabolism and aging interact over time. The damage is comparatively simple, but the details of how that damage spreads and interacts, and how it forms age-related disease, are intricate and poorly understood. We are very complex self-adjusting biochemical factories, so it is a given that even simple malfunctions have complicated outcomes. Because the malfunctions are simple, however, they themselves are the best and most cost-effective point of intervention: the first step towards treatment of aging should be to repair the breakages known to cause it.
The very readable open access paper linked below is a similar argument for engineering (take action now) over science (wait for full understanding), but for less ambitious efforts to intervene in the aging process. These are drug development programs aimed at manipulating the operation of metabolism so as to gently slow the accumulation of damage, and thus slightly slow the pace of degenerative aging. The expected outcome here in terms of additional healthy life delivered per billion dollars invested is not great; you might look at the past decade of sirtuin research to see the median expected outcome, which is to say a lot of data on a tiny slice of metabolism and aging, but no practical therapies. In comparison given a billion dollars and ten years there is a reasonable shot at implementing prototype SENS rejuvenation treatments in mice. The challenge for now is to persuade enough people that this is the best path forward to have a hope of expanding the SENS funding and research community to this scale.
Aging is something everyone can relate to. From grandparents, to parents, and ultimately our own bodies, we are intimately familiar with the declines in form and function that accompany old age. Yet, we don't all appear to age at the same rate. Many individuals are healthy and active well into their 70s, 80s, or even 90s, while others will suffer from chronic disease and disability by the time they reach their 40s or 50s. Those of us that have companion animals also observe that different animal species or even subspecies, as in the case of dog breeds, age at profoundly different rates. Defining the factors that influence individual rates of aging is a major focus of aging research.
From a biomedical perspective, it is critically important to gain a better understanding of the mechanisms that drive biological aging, as age is the single greatest risk factor for the leading causes of death in developed nations. The fact that aging influences so many different conditions is particularly curious. What is it about aging that creates an environment within our cells, tissues, and organs that is permissive for all of these seemingly disparate pathological states?
In order to understand the biological mechanisms of aging, scientists have turned to laboratory model organisms such as rats and mice, fruit flies, nematodes, and even yeast. While some have questioned the utility of these systems as models for human aging, it is now clear that similar pathways and processes affect longevity in each of these species. These studies have resulted in the identification of interventions that slow aging in taxa spanning broad evolutionary distances. Although it is still unknown whether these interventions will slow human aging, the potential impact on human health, if they do, is enormous.
In general, the known conserved modifiers of longevity tend to mediate the relationship between fundamental environmental and physiological cues (i.e., temperature, nutrient status, and oxygen availability) and the regulation of growth and reproduction. One school of thought holds that this relationship results from the ability of organisms to forgo reproduction and invest in somatic maintenance during times of adversity. In other words, based on the quality of the environment, the organism has evolved to make the appropriate choice between allocating its limited resources toward reproducing rapidly, and hence aging more quickly, versus delaying reproduction and allocating resources toward maintaining the soma, thereby aging more slowly.
Although conserved longevity pathways clearly exist, it has been challenging to identify their primary molecular mechanisms of action or even to definitively determine whether they directly modulate the rate of aging. This is true, in part, because there are no generally accepted molecular markers of aging rate in any organism. In mammals, several phenotypes are known to correlate with chronological age, and a handful have been suggested to have some predictive power for future life expectancy; however, none have been demonstrated convincingly in prospective studies.
In addition to gaining an understanding of the molecular mechanisms of aging, a primary goal of aging research is to identify interventions that will slow aging in people. Advanced age is the primary risk factor for the majority of diseases in developed nations, and there are enormous social and financial pressures associated with demographic shifts toward more elderly populations. Interventions that expand the period of healthy life and reduce the period of chronic disease and disability (referred to as "compression of morbidity") offer the potential to alleviate these pressures while simultaneously increasing individual productivity and quality of life.
In practical terms, it may not be necessary to understand in detail why aging is conserved in order to do something about it. In several cases, components of the insulin signaling / mTOR network, as well as the sirtuins, have been shown to be associated with longevity and age-associated disease risk in people. While it remains unclear how difficult it will be to develop interventions to improve healthy aging in humans, there is reason for optimism that this may not be far off. Drugs that target these pathways, including some already shown to increase life span and health span in rodents, are beginning to be tested for effects on age-associated phenotypes or disease in humans. Unfortunately, because of the glacial pace of human aging when compared to common animal models, it will likely take several decades to determine whether rapamycin or other such compounds generally improve age-associated outcomes in people.