Meditations of an oncology geek

Killing Zombie Cells Slows Aging!

without comments

6 November 2011

Original Research Commentary Article

Everyone gets older, but what exactly is aging? Everyone is familiar with getting older (except perhaps if you were born as a character in Huxley’s Brave New World) and is familiar with things associated with aging: wrinkles, diminished organ function, cataracts, and of course, cancer. Readers of my blog are well aware that cancer is an age-related disease.

A very curious article came out this week in Nature, arguably the most prestigious (and stringent) scientific journal. In short, the authors might have discovered a mechanism for HOW aging occurs.

Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.

Now, I’d like to stop there for a second. That’s not usually something you see in reputable scientific journals. On the outset, it sounds more like something that one might hear in science fiction. Good scientists are usually VERY conservative in their extrapolations from their research. To be able to make a statement like that, in one of the most prestigious and vetted scientific journals, takes some serious data.

On a molecular level, aging is associated with increased cellular senescence. A senescent cell can no longer divide and displays diminished biochemical activity. It’s a bit like a Zombie state: neither completely alive or completely dead. Existence without being completely alive. It has been postulated that cellular senescence might be a defense mechanism against aging, or perhaps it is the cause of aging itself? In any instance, senescent cells accumulate in tissues of people undergoing aging.

In an impressive feat of genetic engineering, a team of scientists at the Mayo Clinic programmed all cells that become senescent in a strain of mice to respond to a drug that specifically causes cell death in those cells. In short, these mice will shed all their senescent (Zombie) cells on cue. They developed this gene allele in a strain of mice that have accelerated aging and die very young: about 9 months of age, compared to the usual life span of two years for mice.

So, what happened? The mice given the drug lived longer. Dramatically longer. Getting rid of their senescent cells also caused the mice to keep muscle tissue longer, not thin out their subcutaneous fat stores (the process that gives humans wrinkles) and did not develop cataracts!

The study is now being repeated in a strain of mice that age at a normal pace. It will be interesting to see if these mice live longer than otherwise normal mice.

The drug given to the mice will not work in humans, because no human (to my knowledge) has been genetically engineered to respond to it. But, that does not discount other (undiscovered) drugs or stimuli from doing the same thing.

Could targeting senescent cells slow aging in humans? Maybe. Could other age-related diseases also be thwarted by this anti-senescence approach? Likeā€¦. cancer? It’s exciting to ponder.

-Ryon

Written by Ryon

November 6th, 2011 at 7:38 pm

Posted in Science Blog

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