A fair amount of modern research into aging, longevity and the manipulation thereof starts in studies of the nematode Caenorhabditis elegans. Scientists start with short-lived lower animals such as nematodes, flies and yeast for all the obvious economic reasons; if you're going to pitch an expensive study in mammals - and studies in mammals are always expensive, never mind the ones in which a team carefully monitors the mammals for year after year - you had better have cast-iron support. No-one will fund out of the blue, and working with short-lived, easily managed creatures allows researchers to explore much more of any given problem space at a given level of funding.
One of the benefits of the way the world works - in this case that we all evolved from a common ancestor - is that you can produce value for the development of human medicine from a study of a creature with 1000 cells and lifespan of weeks. There are common mechanisms, shared biochemistry, cellular structures and processes. Here are a couple of recent papers; food for thought, and an insight into some of the work presently underway in the scientific community.
Model organisms have been widely used to study the ageing phenomenon in order to learn about human ageing. Although the phylogenetic diversity between vertebrates and some of the most commonly used model systems could hardly be greater, several mechanisms of life extension are public (common characteristic in divergent species) and likely share a common ancestry. Dietary restriction, reduced IGF-signaling and, seemingly, reduced ROS-induced damage are the best known mechanisms for extending longevity in a variety of organisms.
The nematode Caenorhabditis elegans has proved to be an excellent model organism for the study of development and aging. Many aging mutants have been discovered in the past two decades, and much has been discovered about the physiology of long-lived mutants. It therefore seems surprising that dietary restriction (DR) has not been extensively studied using C. elegans. The main reason for this is the lack of an ideal method to subject C. elegans to DR. However, several authors have tried to study the effect of DR on the metabolism and physiology of C. elegans, and epistasis-type interaction studies have been carried out in order to detect genes that might be involved in DR effects. These studies show that DR life extension is not caused by a reduced metabolic rate, consistent with results in other species. Moreover, the well-known insulin/IGF-1 pathway seems not to mediate life-extending effects. One possibility is that target of rapamycin signaling mediates the effects of DR on life span in C. elegans.
Some folk seem a little skeptical of the whole "target of rapamycin" work, but the proof is in the pudding. Resources continue to pour into the study of calorie restriction biochemistry and the related more general topic of metabolism and longevity - I can't imagine that the most pressing unanswered questions will remain unanswered for too many more years.
The way the mainstream research community is following through on doing something with this new information, on the other hand, seems inefficient - as I've been saying for a while. Greater knowledge eases all future research and development, but some paths forward are better than others:
Practicing calorie restriction is free, but research is not. The present purposing of the aging research community to metabolic manipulation is expensive, but money isn't the real concern. An opportunity is being lost: the real cost is the slowdown in developing a research infrastructure that is instead purposed towards identification and repair of aging damage, a more efficient way forward to extended healthy lives. This is the difference between tuning your engine and taking it to a mechanic: tuning gets you so far and so far only; at some point, you're going to have to repair the components.