The varied approaches to research developed over past decades by the aging research community are driven by two things: firstly that we live for a long time, and secondly the absence of a way to accurately determine an individual's biological age. The only way to measure the effects of potential treatments is to carry out life span studies, and in humans that is impractical to say the least. Thus research into aging and longevity starts with short-lived animals such as nematode worms and flies: exploration and experimentation takes place using these species because life span studies can be carried out in a suitably short period of time to make progress. Promising work moves to mice, where life span studies can last for five years and cost millions. Only later do potential treatments make it to human clinical trials, if at all. This is all much the same as most modern medical research; the process of discovery and development moves incrementally from a state of being far from human biology and cheap to work on to a state of being close to human biology and very expensive to work on.

To a surprising degree the fundamental biology of cells, regulation of metabolism, and mechanisms of aging are similar in even very widely separated species. Aging and many of its interesting epicycles such as the calorie restriction response appeared very early in evolutionary history, a long way down in the tree of life. Thus research in lower animals can still be relevant to human cellular biochemistry, and provide insight into human aging. Nonetheless, worms are not mice and mice are not people. The cost of investigative research that starts with other species is that there is a fair degree of failure when translating promising work over to mammals, and yet more failure when moving from short-lived mammals such as mice to long-lived mammals such as humans. That is acceptable given that the alternative is no research at all, as all studies would be prohibitively expensive to carry out.

Another aspect of research into aging and its associated medical conditions is that genetically altered lineages of laboratory animals are frequently employed. The reasons for this are again economic at root. If you want to study a specific condition, such as old age for example, it is more cost-effective to work with mice that suffer from a DNA repair deficiency that mimics some aspects of accelerated aging than it is to work with normal mice. More research can be carried out more rapidly with accelerated aging mice, even when accounting for the fact that a significantly greater fraction of the results will be irrelevant to normal aging. The same applies to the many different animal models of specific age-related diseases: these are all loose replicas intended to share some characteristics of the disease as it occurs in humans, but under the hood they are not the same thing at all. Animal models are a way to make progress in a cost-effective manner, not an accurate rendition. These things are always worth bearing in mind when reading research results based on animal studies.

Do Model Animals Tell Us Anything about Human Aging?