Transposable Elements are
mobile strands of DNA that insert themselves into Chromosomes (Jumping Genes) with mostly harmful consequences. Cells try to keep them locked down, but Aging cells lose their ability to maintain this control. The consequence may be a further decline in the health of senescent cells and of the Aging bodies they compose.
Even in the level of DNA there is no refuge form rogues that prey on the elderly. Parasitic strands of genetic material the Transposable Elements - transponsones - lurk in Chromosomes, poised to wreak genomic havoc. Cells have evolved ways to defend themselves, but cells lose the ability as they age, possibly resulting in a decline in their function and health.
The chaos that transposons bring can have long-term benefits by increasing genetic diversity in organisms, but in most cases the chaos degrades cell function, such as by disrupting useful genes.
The cell tries to keep transposons quit and keep these things repressed in its genome. However they seem to be barely winning this high-stakes warfare, given that these molecular parasites make up over 40% of the genomes.
Cells try to clamp down on transposons by winding and packing transponson-rich regions of the genome around nucleosomes (little balls of proteins). This confining arrangement makes up the heterochromatin, and the DNA that is trapped in such a tight heterochromatin prison cannot be transcribed and expressed.
Carefully maintaining a heterochromatin prison system is a younger cell's game. Chromatin changes profoundly with Aging. Young and spry cells distinctly maintain open "euchromatin" formations in regions where essential genes are located and closed "heterochromatin" formations around areas with active transposable elements and a few desirable genes.
The distinction appears to become worn in Aging, or senescent cells. Chromatin tat once is open tend to become more closed and the chromatin that is once closed, tend to become more open.
Genomes contain well over a million copies of transposable elements that are very similar to one another. The chromatin lockdown is breaking down and the newly freed transponsons are taking full advantage.
All these transposable elements start to get expressed and actually start moving around to other regions in the genome.
The relevance of the damage that the cells suffer from the transposable element jailbreak and resulting genetic crime spree is not clear. It depends on the timing. The transposition may really bad for the organism or it it may be something that happens so late that by that point the organism has already accumulated so much age-associated damage and then this extra insult of transposition is not going to make a lot of difference.
Drugs might be able to suppress transposons in Aging cells. Virtually all the transposons of concern in mammals are "retrotransposons" because they use RNA and an enzyme to copy themselves. Certain HV drugs inhibit this reverse transcriptase. The reverse transcriptase of the major human retrotransposons "L1" are inhibited by some HIV drugs widely used in the clinic. Dugs that highly specifically target L1 might be considered to be tested for anti-Aging effects.
The ultimate success would provide a way to restore order in the cells and forstall at least some of the molecular ravages of age .