A post at Extreme Longevity touches on an area of interest in aging research, and comes with a link to a PDF versions of the paper in question. It is another study confirming the link between levels of the protein p16INK4A and aging, something that has been known for some years. In particular, it shows up in the senescent cells that accumulate with age, something that researchers have managed to make use of: you might recall last year's study that showed beneficial effects from destroying senescent cells in rats. That research group used p16INK4A as a basis for their method of selective destruction, targeting only those cells that had become senescent and thus removing their contribution to the aging process.

It is worth noting that p16INK4A is a gene with a lot of aliases - which tends to happen when many different researchers have been working on the biochemistry independently. The official name is CDKN2A, or cyclin-dependent kinase inhibitor 2A, but it can be referred to as p16 as well. In any case, here is the Extreme Longevity post, a PubMed reference, and the PDF version of the paper:

In this study the researchers examined skin cells from middle aged people aged 43 to 63. They compared a group who had a strongly family history of extreme longevity to age-matched controls. They found that p16 expression in skin cells was significantly lower in the group that had the strong family history of longevity. They conclude "a younger biological age associates with lower levels of p16INK4a positive cells in human skin."

This study supports the idea that p16 expressing cells are linked to age both from a chronological as well as biological perspective. Work needs to be done to find a way to remove p16 positive cells from all tissues of the body on a regular basis. Such a therapy, if it existed, may act to reduce aging.

This all ties back in to cancer suppression versus tissue proliferation. Increased senescence in cells is one way of biasing the average over time to a lower rate of cancer - because the cells most likely to cause issues have been taken out of circulation and are no longer replicating. They should be destroyed by the immune system, but the immune system has its own age-related issues and falls down on that job, leaving the senescent cells to lurk and emit harmful signaling chemicals that damage surrounding tissue.

The flip side of the coin is that less replication among cells translates to less resilient tissues and organs, and thus faster aging. As mammalian biochemistry is set up by default, you can either be generating lots of fresh cells with a higher cancer risk, or aging faster due to poor tissue maintenance, but with a lower cancer risk. Biotechnology will let us escape from this Hobson's choice in due course - a method for tweaking the system associated with another cancer suppression gene to generate both less cancer and slower aging has been demonstrated in mice, for example. More and better technologies will emerge in human medicine in the fullness of time.

In particular, rather than focusing on metabolic tinkering to incrementally improve matters, the better approaches would be to (a) repair the ability of the immune system to eliminate senescent cells at a youthful level, and (b) develop therapies to regularly completely sweep senescent cells from the body. The effects of reducing senescent cell numbers in rats were sufficiently good that more work will be devoted to that sort of strategy in the future - and a good thing too.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm