Last week Nature published the research of scientists from Harvard Medical School into the impact of telomerase reactivation on ageing in mice that were engineered to have short, dysfunctional telomeres. Amazingly, this process is able to reverse ageing in mice which are in an advanced stage of degeneration, indicating that reactivating telomerase may one day become an effective therapy to counter age-related degeneration in humans.
Telomeres are repetitive sequences of DNA on the ends of each chromosome that act as protective caps for the genetic information in the main body of the chromosome. It has long been understood that telomeres play a role in cellular ageing. The process of DNA replication leaves out the outermost edges of the telomere, reducing the length of the telomere in the new copy of the chromosome. After a certain number of cell cycles, the telomeres shorten to a critical length that prevents further cell division and the cells become senescent. In the case of the engineered mice, having short telomeres from the beginning meant that the process of cell ageing and senescence occurred more rapidly. As more cells become senescent and die off, tissues begin to atrophy and the function of organs begins to decline. This produces the degenerative effects associated with ageing
Reversing this process is a key factor in extending lifespan. The way to do this is well understood. The enzyme telomerase reverses telomere shortening by re-adding the length of DNA lost from the telomere cap during DNA replication. This allows the elongation of the telomere such that the cell does not enter senescence and can continue to divide. Until now, it was not understood how big an impact telomerase reactivation could have in an organism that was in an advanced stage of ageing. This research showed that after the reactivation of telomerase resulted in the regeneration of healthy tissue, improved organ function and an increased life span.
Though this development is remarkable, it must be taken with some caution. The activation of telomerase is a mechanism essential to the proliferation of cancerous cells. Thus, there is a balance that needs to be considered between the halting and reversing of degeneration and an increased risk of developing cancer.
