Telomerase and Aging in the News Again, But Not For Any Good Reason

The social media communities and mainstream media have been abuzz over a recently released study on telomerase and aging in mice. For my part, I think that this is nothing more than a good example of the random and at times self-defeating way in which research is publicized and then catches the public eye. A short summary of the study is as follows:

At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.

You might look back into the Fight Aging! archives for a primer on the intersection of telomeres, telomerase, and aging. It's interesting stuff, but unfortunately this present research is being headlined as "scientists reverse aging in mice" - which is absolutely not what was accomplished. Reversing an artificially created accelerating aging condition by removing its cause is not the same thing as intervening in normal aging, and it will rarely have any relevance to normal aging. The study results are teaching us something about the way in which telomerase works in mouse metabolism, but I - and other, more qualified folk - are dubious as to the relevance to human aging:

The goal for human tissue 'rejuvenation' would be to remove senescent cells, or else compensate for the deleterious effects they have on tissues and organs. Although this is a fascinating study, it must be remembered that mice are not little men, particularly with regard to their telomeres, and it remains unclear whether a similar telomerase reactivation in adult humans would lead to the removal of senescent cells.

The bottom line is that it is really only worth getting excited over a study that shows extension of life rather than an un-shortening of life. It's all too easy to create short-lived mice and then make them less short-lived - hundreds of studies have achieved this result in one way or another. Also bear in mind that the media and public at large don't tend to seize upon one specific research result above another for any rational reasons. When it comes to what is shouted from the loudspeakers on a given day, it's all a matter of accident and marketing rather than facts and understanding. For example, you might recall that telomerase and p53 were used to extend normal mouse life span by 50% a few years ago - far more important and interesting than this present study, yet it received next to no attention.

The Harvard researchers responsible for the accelerated aging and telomerase study in mice we're discussing today will go on to look at extended longevity:

The team is now investigating whether it extends the lifespan of mice or enables them to live healthier lives into old age.

If they find some way to boost the normal life span of mice, then we might pay more attention. But for now the circus treatment is unwarranted.