This article goes into some detail on recent research into whether retrotransposons in the genome play a meaningful role in aging. This is analogous to the debate over whether stochastic nuclear DNA damage has a role in aging beyond causing cancer, and the sort of studies you'd need to introduce clear proof one way or another are much the same:
Retrotransposons, often referred to as jumping genes, are mobile genetic elements that parasitize host machinery to replicate themselves across the genome. Since their emergence more than 100 million years ago, retrotransposons have been enormously successful. Modern mammalian genomes, for example, are riddled with the scars of these copy-and-paste events, with retrotransposon-derived DNA now accounting for nearly 50 percent of the human genome.
The most dangerous retrotransposon in mammalian genomes is the long interspersed nuclear element-1 (LINE-1 or L1). L1 retrotransposons are a little more than 6 kilobases long and encode an RNA-binding protein and an endonuclease with reverse-transcriptase activity that allow the element to autonomously replicate in the host genome via an RNA intermediate. The human genome contains more than 500,000 copies of L1s. Although the vast majority of these have been inactivated as a result of truncation, mutation, and internal rearrangement, it is estimated that approximately 100 of these L1s per nuclear genome still retain their replication activity. Despite their abundance, however, L1s are not benign. Rather, their activity, and even their presence, represents a real danger to the host, increasing the risk of DNA damage, cancer, and other maladies. Given the consequences of L1 activity, it is unsurprising that host genomes devote considerable resources to suppressing these retrotransposons. Indeed, every step of the L1 life cycle is impeded in some way by host factors such as gene silencing, antiviral defense machinery, small RNAs, and autophagy.
Historically, little attention has been given to retrotransposition in somatic tissue, because this was thought of as an evolutionary dead end. In recent years, however, evidence has accumulated that L1 elements can become active in a variety of somatic tissues in humans and mice, including in the brain, skeletal muscle, heart, and liver. Intriguingly, some of the highest L1 activity has been observed in aging tissues, particularly those affected by age-related pathologies such as cancer. This raises the interesting possibility that L1 activity may contribute to the aging process. Increased DNA damage and mutagenesis are prevalent in aging tissues, and L1 activity is known to increase following such damage. In addition, a small number of studies have shown that overexpression of L1 can cause cells to senesce, a hallmark of aging tissues. The role of L1 in driving age-related processes is now a topic ripe for study.