One of the hurdles in the way of better understanding the root causes of aging is that it is extremely challenging to change any one piece of cellular machinery in isolation. Evolution has produced structures and processes that promiscuously reuse one another's building blocks, so alter a gene or add a protein and it will affect all sorts of different mechanisms inside the cell, which will in turn cascade to cause further changes.
In the case of telomeres there is some debate over whether the diminished telomere length associated with aging and ill health is a primary cause of aging or a secondary effect. Using telomerase to lengthen telomeres extends life in mice, but telomerase has other effects as well. Average telomere length can vary up and down over the short term in any given tissue in the body, and these telomere dynamics are quite different in different species.
The ways forward towards a better understanding of the role of telomere length in aging include implementing rejuvenation biotechnologies such as SENS to see what the effects are on telomere length, or finding ways to extend telomeres without producing any other changes in a cell:
It is well known in the scientific community that telomeres shorten every time a cell divides and eventually become so short that they can no longer protect the chromosomes. The unprotected chromosome ends send signals that stop the cell from dividing further, a state referred to as "senescence". Senescent cells occur more frequently as we age, which can contribute to tissue loss and organ failure.
[Researchers have] now discovered that turning transcription on or off at telomeres can have drastic effects on their length. Transcription is the process of making an RNA molecule from DNA. It has only recently been shown to occur at telomeres, but the functional significance of this discovery has remained a mystery. Molecular biologists [were] now able to show that the RNA itself is the key regulator that drives telomere length changes, especially when it sticks to telomeric DNA to make a so-called "RNA-DNA hybrid molecule".
"We experimentally changed the amount of RNA-DNA hybrids at the chromosome ends. We can thus either accelerate or diminish the rate of cellular senescence directly by affecting telomere length." This could be a first step towards telomere-based therapies for tissue loss or organ failure. With respect to diseases, it remains to be determined whether altering transcription rates at telomeres does indeed improve health status. This approach is also significant for cancer cells, which do not senesce and are thus considered immortal. "Transcription-based telomere length control may therefore also be applicable to cancer treatment."