The initiation of diseases associated with aging, such as cancer, is largely attributed to DNA, or genetic, damage. But this study suggests that aging itself is infinitely complex: that progressive telomere shortening hastens chromosomal aging by changing the way genes entwine with histones, so-called "epigenetic" changes. How DNA interacts with histones has enormous impact on whether genes are expressed-hence the current intense interest in the relationship of the epigenomic landscape to disease states.

Rescue experiments in which the team cosmetically enhanced aging cells confirmed that signals emitted by eroding telomeres drove epigenetic changes. When aging cells were engineered to express telomerase, the enzyme that restores and extends stubby telomeres, those rejuvenated cells showed histone levels reminiscent of "happy, healthy chromatin," and a partial return to a youthful chromatin profile.

Lest you sink your savings into schemes to elongate your telomeres, beware. "The flip side of elongating telomeres is that you enable cells to grow for much longer periods and can generate what are called "immortal" cells," says Karlseder. "That takes you one step closer to cancer cell development."

Up to now, the Karlseder lab has mostly focused on interactions between telomeres and DNA repair mechanisms. This paper now pushes them into the field of epigenetics. "We will continue to examine epigenetic changes in cells at different ages," says Karlseder. "We now want to determine if histone changes follow a linear process or whether they kick in as we age."

Source: Salk Institute