Posted by admin at 8:12 PM Tuesday, March 30, 2010
How many of us would like to hear something like that from their doctor? Probably most. But is it really possible to devise a drug that will make you live longer? You may be surprised that the answer is “probably”, and in fact we seem to not be very far from developing one. In July 2009, Harrison et al.(1) reported in Nature that feeding middle-aged mice a drug called rapamycin significantly extended their lifetime, regardless of their genetic background.
This incredible breakthrough was possible because of a radical revolution that is happening in the field of aging biology. For a long time it was thought that aging was simply a result of wear and tear brought about by reactive oxygen species, molecules that form naturally in each of our cells as a result of our aerobic metabolism(2). However, now a dramatically different paradigm is replacing the wear and tear view. Though it is still regarded as possible that reactive oxygen species are somehow involved in the aging process, most scientists now regard aging as a programmed event which can be seen as an extension of normal development. If this is indeed the case, specific inhibitors of key enzymes in the pathway should be able to increase lifespan, much like antiretrovirals postpone the progression of AIDS.
One of the biochemical pathways that have surfaced in recent years as a key player in the aging process is the so-called TOR pathway, at the heart of which lies an enzyme known as the TOR kinase. By inhibiting the TOR pathway, researchers have successfully extended the lifespan of organisms as diverse as brewer’s yeast(3), nematodes(4) and fruitflies(5). Until now, however, it was not known if this was possible in mammals because mammals do not possess the TOR kinase, though they do have a related enzyme referred to as mTOR. Now, Harrison et al. prove that feeding an mTOR inhibitor (rapamycin) to mice late in their life increases lifespan by as much as 14%.
This study holds great promise for increasing human life span for a number of reasons. Firstly, the authors used genetically heterogeneous mice, as opposed to the usual highly-inbred laboratory mice. This is a crucial distinction, because inbred strains usually die of a particular disease, while “normal” mice, like people, die of various causes. Thus rapamycin does not only decrease the risk of a particular disease, it is a real inhibitor of aging. This is further supported by the disease profile of rapamycin-fed mice, which was identical to that of control mice. Secondly, the rapamycin was fed late in the life of the mice. This means that – in case this is ever confirmed in humans – each individual could choose if he or she wants to live longer.
Thus, it seems that the new paradigm is paying off. Of course, results like these need to be confirmed, and there must be a certainty that administering rapamycin to humans does not have any serious side effects. If this turns out to be the case, it may not be so unrealistic to hope that in twenty years clinical trials for a scientific fountain of youth will be underway.
- S. Andrei Anghel
[From September 10, 2009]
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