The many types of advanced glycation endproducts, or AGEs, build up with age. These are forms of sugary gunk that glue together important components in your cellular machinery, and enough of that going on would ultimately become a fatal problem. AGE levels are probably (for most people) more of a contributory cause than principle cause of age-related degeneration, however. The other things kill you first - but it's all a matter of accumulation, and every form of unrepaired biological damage plays its part in hastening the end.
It is likely that the way in which AGEs cause issues has just as much to do with making cells act in counterproductive ways as it does with outright destruction of essential mechanisms. An important focus of research is RAGE, the cellular receptor for AGEs, which is involved in the inflammatory response. As I'm sure you know by now, chronic inflammation is very bad for you over the long term, and goes a long way towards degrading health and remaining longevity. If your body is flooded with AGEs, then one consequence is inflammation - and that in turn will cause harm over time in many different ways.
The picture of AGEs and aging is already complicated by diet - some AGE levels are very variable, and depend on what you happen to be eating - and metabolic conditions such as diabetes wherein the overall behavior of human metabolism is quite different from that of an aged but otherwise normal person. Much of the modern populace eats far too much, and far too much sugar as well, which leads to these sorts of conditions of overnutrition.
Today I noticed an open access paper that adds another layer of complexity to the picture of AGEs and aging. Bacteria produce AGEs, and RAGE and its connection to the inflammatory response may be a component part of the immune system - a mechanism that evolved long before we humans had ready access to the damaging levels and types of food we presently consume.
Advanced Glycated End Products (AGEs) are formed by non-enzymatic protein glycation and are implicated in several physiological aspects including cell aging and diseases. Recent data indicate that bacteria - although short lived - produce, metabolize and accumulate AGEs. Here we show that Escherichia coli cells secrete AGEs by the energy-dependent efflux pump systems. Moreover, we show that in the presence of these AGEs there is an upshift of pro-inflammatory cytokines by mammalian cells.
Thus, we propose that secretion of AGEs by bacteria is a novel avenue of bacterial-induced inflammation which is potentially important in the pathophysiology of bacterial infections. Moreover, the sensing of AGEs by the host cells may constitute a warning system for the presence of bacteria.
So in short, it would seem plausible that the reaction to accumulating AGEs is yet another way in which both modern overnutrition and the established course of aging act separately but combine to sabotage the evolved workings of the immune system. We already know that the immune system is formed to be very efficient in youth but structurally fails over time, so one more mechanism that follows this pattern shouldn't be too surprising.
The only good news here is that safely getting rid of AGEs should be one of the least challenging aspects of aging for the present pharmaceutical research and development community to tackle over the next few decades - as and when they get around to deciding that they should be working on that. Producing drugs, bioremediation therapies, or immune therapies to break down specific forms of unwanted chemical will soon enough be the core competency of the pharmaceutical industry.