Transposable elements are parasitic DNA sequences that have attached themselves to the genome over the course of evolutionary history. They are rigorously suppressed in normal cellular operation, but that suppression appears to fail with age, leading more cells to suffer replication of these transposable elements. This activity shows up in senescent cells, for example.
Some researchers, such as the authors of the paper linked here, argue that rising activity of retrotransposons - or transposable elements - in our DNA are a cause of aging. This is a subgroup of those who think that, more generally, accumulated stochastic nuclear DNA damage is a cause of aging above and beyond paving the way to higher levels of cancer. It is thought to disarray the activities of cells to a large enough degree to disrupt tissue function. As for transposable elements, the data can be argued either way: while the correlations are strong and DNA damage is shown to raise cancer risk, there is no good experimental evidence to demonstrate that nuclear DNA damage in isolation significantly contributes to aging in other ways across the current length of a human life span, nor to definitively answer the question of whether transposable element mobilization is closer to being a root cause or closer to being an end consequence in aging.
As in many of these mechanisms, the best and fastest approach to obtaining that answer would be to repair the damage and see what happens - assuming that repair to be feasible. For stochastic DNA damage, this is becoming somewhat more practical as a future possibility with the falling cost of gene therapy and improved techniques such as CRISPR, but the challenge here is substantial: how to fix different forms of damage in every cell. Short of full-blown molecular nanotechnology, the development of complex programmable machines built of DNA or similar, capable of figuring out what to fix in situ inside a cell, I see few options.
Understanding the molecular basis of ageing remains a fundamental problem in biology. In multicellular organisms, while somatic tissue undergoes a progressive deterioration over the lifespan, the germ line is essentially immortal as it interconnects the subsequent generations. Genomic instability in somatic cells increases with age, and accumulating evidence indicates that the disintegration of somatic genomes is accompanied by the mobilisation of transposable elements (TEs) that, when mobilised, can be mutagenic by disrupting coding or regulatory sequences. In contrast, TEs are effectively silenced in the germ line by the Piwi-piRNA system.
Here, we propose that TE repression transmits the persistent proliferation capacity and the non-ageing phenotype (e.g., preservation of genomic integrity) of the germ line. The Piwi-piRNA pathway also operates in tumorous cells and in somatic cells of certain organisms, including hydras, which likewise exhibit immortality. However, in somatic cells lacking the Piwi-piRNA pathway, gradual chromatin decondensation increasingly allows the mobilisation of TEs as the organism ages. This can explain why the mortality rate rises exponentially throughout the adult life in most animal species, including humans.