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What causes cells to age?
 

The future of research into cellular senescence
 
The potential to learn more about aging, longevity determination and the diseases of old age by studying cultured normal and cancerous human cells is enormous. Here are some examples of present research directions:

The reason that cancer cells are immortal is that, unlike normal cells, they produce an enzyme called telomerase that maintains their telomeres at a constant length. This prevents a diminishing length from triggering the cell to stop dividing as it does in normal cells. Because telomerase is found almost exclusively in cancer cells, a search is on for chemical inhibitors of telomerase. An inhibitor, if found, could be useful in preventing the further replication of cancer cells.

In a discovery made two years ago, it was demonstrated that normal mortal human cells could be made immortal by using a procedure that made the normal cells switch on the production of their telomerase enzymes. These normal human cells became immortal yet still retained their normal properties. The potential use of this technique is great, making it possible to produce normal human cells on a large scale and enabling the cells themselves or the products they produce to be used for a variety of therapeutic purposes.

Tests being developed for the presence of telomerase are so sensitive that single cancer cells can be detected in body fluids like urine and saliva. This could provide opportunities for much earlier detection of bladder and lung cancer cells. Telomerase expression in cancer cells is the single most specific difference yet found between normal and cancer cells.

The goal of research on the phenomenon of cellular senescence is not unlike the goal of all research on the biology of aging. It is not to make us all immortal; that is not only impossible but also undesirable. Nor is it to stop or slow down the processes of aging, because those processes are inevitable. And because the determinants of our longevity are driven indirectly by most, if not all, of our genes, it is also very unlikely that tampering with that process is either probable or even desirable.

Instead, our goal in this research and other research in the field of aging should first be to understand why old cells are more vulnerable to disease than are young cells. Once accomplished, those differences, if exploitable, could result in a maximum 15-year increase in human life expectation. Then the underlying inexorable processes of aging will be revealed as the cause of death. Unfortunately, those processes, absent the replacement of all vital organs--including the improbable replacement of the brain--will almost certainly be inescapable.




 
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