You might recall a recent article on transposons as a form of more aggressive genetic damage and disarray in the later stages of aging. It is unclear as to whether this is a secondary effect or whether it does in fact contribute to age-related decline at that stage; the arguments would be much the same as those made for other forms of stochastic DNA damage in aging. Here is another example of recently published research on transposons and aging:
[Researchers] showed that when the activity of a protein called Ago2 (Argonaute 2) was perturbed, so was long-term memory [in fruit flies] - which was tested using a trained Pavolvian response to smell. Since Ago2 is known to be involved in protecting against transposon activity in fruit flies, [the scientists] were compelled to look for transposons. Though transposons have been shown to be active during normal brain development, they are silenced soon afterward. The implication is that they have some functional role in development.
When [the team] looked for transposons they found that there is a marked increase in transposon levels in the brain cells, or neurons, by 21 days of age in normal fruit flies. The levels were observed to increase steadily with age. These transposons, including one in particular called gypsy, were highly active, jumping from place to place in the genome. When they blocked Ago2 from being expressed in fruit flies, transposons accumulated at a much younger age.
Accompanying this transposon accumulation were defects in long-term memory that mirrored those usually seen in much older flies, as well as a much-reduced lifespan. "Essentially the Ago2 knock out flies have no long-term memory by the time they are 20 days old, while normal flies have a normal long-term memory at the same age." [The researchers propose] that a "transposon storm" may be responsible for age-related neurodegeneration as well as the pathology seen in some neurodegenerative disorders.
However, [the] studies so far don't address whether transposons are the cause or an effect of aging-related brain defects. "The next step will be to activate transposons by genetically manipulating fruit flies and ask whether they are a direct cause of neurodegeneration."
The challenge with this sort of research is that it's easy to exhibit reduced life span by pulling out necessary parts of an animal's biochemistry, but very hard to show that this is actually relevant to aging versus just another form of causing damage. The real test in this case would be to find a way to suppress transposons with minimal other changes to biochemistry and show extended life - or at least preserved cognitive function - as a result. That would be compelling.