Transposable elements make up a sizable portions of the genome, capable of copying themselves to other locations in the genome under the right circumstances. This activity is suppressed in youth, but increases in older individuals for reasons that are still being explored. Transposable element activity is thought to contribute to aging in a similar way to the effects of mutational damage to DNA, setting aside the risk of cancer, meaning a growing disarray in cellular metabolism due to altered genes and gene expression. When this occurs in stem cells or progenitor cells, this disarray might propagate to a sizable fraction of cells in a tissue.

It is still a little early to say to what degree transposable element activity is a problem, in comparison to the other contributing mechanisms of aging, and what the best approach to suppress it might be. Nonetheless, it is worth considering the recent research suggesting that the operation of DNA repair processes that address double-strand breaks in the nuclear genome causes epigenetic changes characteristic of aging. The LINE-1 retrotransposons have been shown to increase the pace at which double-strand breaks occur once they become active. Joining the dots, perhaps this is a plausible mechanism for cellular disarray. It is an interesting connection, but one that needs further exploration and validation, however.

The role of transposable elements activity in aging and their possible involvement in laminopathic diseases