In recent years a number of researchers have used blood transfusions and mixing to discover and investigate systematic differences in biochemistry between old and young mammals. Many of the body's distributed systems use the circulatory system as a means of carrying signals and instructions throughout the body. Thus introducing old blood into the young or young blood into the old can bring about measurable biochemical changes that tell us more about the specific changes that occur with aging.
Aging is damage, but all of our biological systems are highly responsive to changing circumstances - so where there is damage, there will also be an evolved response to that damage. In theory that will be a coping response, but what evolution considers "coping" might not match with your opinions on the subject. For example, one form of characteristic response that occurs as we age is a progressive diminishing of growth and repair: stem cell populations stop doing their jobs as enthusiastically, for example, and the quality of our tissues suffers for it. It reduces the risk of cancer, but that's cold comfort for someone who is effectively being worn away, every bodily structure decaying faster than it is being repaired.
But back to the blood: here is a fresh example of what can be learned from mixing the blood of mice.
Stanford University School of Medicine scientists have found substances in the blood of old mice that makes young brains act older. These substances, whose levels rise with increasing age, appear to inhibit the brain's ability to produce new nerve cells critical to memory and learning. ... An early step in the Stanford team's study involved connecting the circulatory systems of pairs of old and young mice via a surgical procedure, so that blood from the two mice comingled. "This way, we could examine the effects of old mice's blood on young mice's brains, and vice versa. ... We saw a threefold increase in the number of new nerve cells being generated in old mice exposed to this 'younger' environment." ... In contrast, the young members of old/young mouse pairs exhibited fewer new nerve cells in the dentate gyrus than did young mice untethered to elders.
To identify specific circulating factors associated with aging and tissue degeneration or tissue regeneration, the researchers assayed 66 different immune-signaling proteins found in mice's blood. Six of these factors were elevated in both unpaired old mice and young mice that had been paired with older ones. At the top of the list was eotaxin, a small protein that attracts a certain type of immune cells to areas where it has been secreted by other types of cells. Highlighting this discovery's possible relevance to humans, [tests] conducted on blood and cerebrospinal fluid samples drawn from healthy people between the ages of 20 and 90 showed a parallel age-related increase in eotaxin.
Much of today's research is channeled into what is effectively a process of trying to patch over damage: the fastest way to try to move from laboratory to building something that the FDA might actually allow into the clinic is to (a) identify a single component is a biological system that might be manipulated to some palliative effect, then (b) design a drug to manipulate it with as few side-effects as possible. This two-step process is what much of the pharmaceutical industry and regulatory bodies are geared up for, and all they recognize. Try to do something different and your path will be longer and more challenging - see, for example, the fact that early stage stem cell therapies still cannot be obtained in US clinics, despite having been available overseas for a number of years now.
My point here being that work like that quoted above is interesting as a potential foundation for a way to patch over some of the issues that crop up with aging - but patching is a very different matter from repairing root causes, and will always ultimately fail. If better ways ahead are possible, and they are, then strategies involving patching should take second place in the priority queue.