Telomeres are ‘tag ends’ of our DNA chromosomes. In the process of reproducing cells, the telomere signals where to stop transcribing genes. However, during the process of mitosis, when the DNA duplicates and a new cell is created, sometimes the telomere is cut (snipped) before the end. It becomes shorter. Eventually there may be no telomere remaining, and the cell will fail to replicate. This has been shown to relate to the aging process (SciTechStory, November 9, 2009: Study confirms telomere’s role in living longer).

Normally DNA attempts to keep the chromosomal telomeres at the proper length. In fact, it has at least one gene associated with the task: telomerase RNA component or TERC. The research shows that some people have variations, either in TERC or genes associated with it that prevent TERC from working properly. These people age early, or fall prey to diseases of old age earlier.

Professor Tim Spector from King’s College London and director of the TwinsUK study, who co-led this project, added:

“The variants identified lies near a gene called TERC which is already known to play an important role in maintaining telomere length. What our study suggests is that some people are genetically programmed to age at a faster rate. The effect was quite considerable in those with the variant, equivalent to between 3-4 years of ‘biological aging” as measured by telomere length loss. Alternatively genetically susceptible people may age even faster when exposed to proven ‘bad’ environments for telomeres like smoking, obesity or lack of exercise – and end up several years biologically older or succumbing to more age-related diseases. ”

[Source: EurekAlert]

Identification of the variant genes is, of course, just a start. Analyzing the relationship between ‘normal’ and ‘variant’ genes and how they affect the reproduction of telomeres is a next step. As with much of the work on gerontology – this avenue of approach is many years away from producing something to counteract the effects of aging.