Telomeres are the ends of the chromosome, caps of repeating DNA sequences that shorten with each cell division and lengthen according to the activity of the enzyme telomerase - this is a very dynamic process, responding differently to circumstances in different cells and tissue types. Telomere length somewhat acts as a countdown clock, moving a cell towards shutdown after a certain number of divisions rather than permitting continued replication, but as for all matters biological the telomere-telomerase-chromosome system considered as a whole is exceedingly complex. It influences and is influenced by many other important cellular systems and feedback loops: mitochondrial damage, for example, appears tied to telomere length and telomerase activity. Thus even as data rolls in ever faster in this age of biotechnology, the telomere story has stubbornly remained that telomeres generally become shorter on average with age or ill health or stress, and that this shortening might be a contribution to aging or it might only be a marker for other cellular changes and damage that occurs with aging.
This is an important distinction to draw: we should find ways to fix and reverse the changes that are fundamental, that are causes of aging. But we don't have to fix and reverse the markers and secondary changes. If we repair the root causes, the many other line items should take care of themselves. But biology is complicated - obtaining the answers for processes that are right down there in the depths of the cellular machinery, central to everything and touching on everything, takes time.
Here's a good editorial from Impact Aging, very readable for the layperson:
Not surprisingly, given that species differ in many other relevant aspects of their biology, including the pattern of activity of the telomere-restoring enzyme telomerase simple comparisons of average telomere length across species do not map directly onto interspecific variation in maximum lifespan. In relatively long-lived species, telomerase is downregulated in most somatic cells, thought to have evolved as a mechanism to counteract an increased risk of tumour formation, particularly in endotherms. One potential cost of this is that tissue renewal capacity is limited, resulting in somatic deterioration with age.
However, within a given long-lived species, there is good reason to predict that variation in average telomere length in somatic cells will be related to potential lifespan. Examining this link is fraught with difficulties, not least of which is that studies covering the entire lifespan of a cohort of long lived animals take a very long time. Circumventing this by looking at telomere length and subsequent survival in individuals that are already old omits all the individuals who died early in life (and who may have had the shortest telomeres). The alternative approach of comparing average telomere length in a cross sectional sample of individuals of different ages suffers from a related bias; mean telomere length could actually appear to increase with age if individuals with short telomeres die and so drop out of the sample. Furthermore, since telomere length is a dynamic character, if it is predictive of lifespan, we also need to know at what life history stage the relationship is strongest. Longitudinal studies are therefore essential.
Time is the most precious thing for us, and it is unfortunate that finding the necessary information that would allow the research community to be more effective in addressing the causes of aging - by eliminating potential mechanisms from the "must fix" list - might at this point take up more time than it would save.