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PORTSIDE  November 2011, Week 1

PORTSIDE November 2011, Week 1

Subject:

First Proof That Senescent Cells Can Drive Aging Process

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Date:

Sun, 6 Nov 2011 22:59:28 -0500

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Purging Cells in Mice Is Found to Combat Aging Ills
By NICHOLAS WADE
New York Times
November 2, 2011
http://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html

In a potentially fundamental advance, researchers have
opened up a novel approach to combating the effects of
aging with the discovery that a special category of
cells, known as senescent cells, are bad actors that
promote the aging of the tissues. Cleansing the body of
the cells, they hope, could postpone many of the
diseases of aging. 

The findings raise the prospect that any therapy that
rids the body of senescent cells would protect it from
the ravages of aging. But many more tests will be needed
before scientists know if drugs can be developed to help
people live longer.

Senescent cells accumulate in aging tissues, like
arthritic knees, cataracts and the plaque that may line
elderly arteries. The cells secrete agents that
stimulate the immune system and cause low-level
inflammation. Until now, there has been no way to tell
if the presence of the cells is good, bad or
indifferent.

The answer turns out to be that the cells hasten aging
in the tissues in which they accumulate. In a delicate
feat of genetic engineering, a research team led by
Darren J. Baker and Jan M. van Deursen at the Mayo
Clinic in Rochester, Minn., has generated a strain of
mouse in which all the senescent cells can be purged by
giving the mice a drug that forces the cells to self-
destruct.

Rid of the senescent cells, the Mayo Clinic researchers
reported online Wednesday in the journal Nature, the
mice's tissues showed a major improvement in the usual
burden of age-related disorders. They did not develop
cataracts, avoided the usual wasting of muscle with age,
and could exercise much longer on a mouse treadmill.
They retained the fat layers in the skin that usually
thin out with age and, in people, cause wrinkling.

"I am very excited by the results," said Dr. Norman E.
Sharpless, an expert on aging at the University of North
Carolina. "It suggests therapies that might work in real
patients," he said.

Dr. van Deursen's work is the first to show that
removing senescent cells is beneficial. If confirmed, it
"will be considered a fundamental advance by our field,"
Dr. Sharpless said.

Aging research is a relatively young field because until
20 or so years ago the prospect of defeating age seemed
hopeless. Then researchers found that the lifespan of
laboratory animals could be extended by manipulating
certain genes, setting off a hunt for drugs that might
influence the corresponding genes in people. This line
of research remains promising but has produced few
tangible results so far. The discovery that senescent
cells seem to be the cause of tissue degeneration opens
out a new direction for researchers on aging to explore.

Judith Campisi, at the Buck Institute for Research on
Aging, said the new finding was the first proof that
senescent cells can drive the aging process. "So it's
really quite a breakthrough," she said.

In both mice and people, senescent cells are few in
number but have major effects on the body's tissues.
Killing the cells should therefore have large benefits
with little downside. The gene-altering approach used on
the mice cannot be tried in people, but now that
senescent cells appear to be harmful, researchers can
devise ways of targeting them.

Drugs already exist to combat some of the inflammatory
hormones secreted by senescent cells. The body's immune
system, which probably clears away senescent cells all
the time but does so less efficiently with age, could
perhaps be trained to attack senescent cells more
aggressively. Or researchers could one day develop
specific drugs to kill the cells, when the differences
between ordinary and senescent cells are better
understood.

Dr. van Deursen said he thought it worth trying to
eliminate senescent cells after the finding that they
reliably switch on a characteristic marker gene known as
p16-Ink4a. In his mice, he arranged that the genetic
element that switches on the marker gene would also
prime a mechanism to make the cell self-destruct. The
mechanism fired only when the mice were dosed with a
specific drug. The result was that only senescent cells
were at risk from the drug, and that they could be
purged at any desired time in the mouse's lifetime.

In a second experiment, the mice were not given the
cell-cleaning drug until they were middle-aged. Their
cataracts had already developed by then and were
irreversible, but aging was delayed in their fat and
muscle tissues.

It may be that senescent cells are beneficial in youth
but harmful in old age, when the immune system seems to
clear them less rapidly from the body. The second mouse
experiment suggests that middle age would be an
effective time for clinical intervention, assuming
humans behave in the same way.

If aging of the tissues is delayed by eliminating
senescent cells, the mice should, in principle, have
lived longer. Dr. van Deursen said this was not the case
in this experiment only because he had chosen a fast-
aging strain of mice in order to save himself time.
These particular mice succumb to heart attacks at an
early age, regardless of the state of their tissues. The
Mayo Clinic team plans to repeat its experiment with an
ordinary strain of mouse that normally lives three years
or more, to see if its life span is extended as
expected.

The Mayo Clinic finding "is a really important step
forward for the field," said Dr. Campisi of the Buck
Institute.

The purpose of research on aging, she said, is not to
let people live a thousand years, as portrayed in
science fiction, but to increase health span, the
proportion of people's natural lives that they live in
good health.

"People used to see aging as a rusting nail -- there's
nothing you can do about it," Dr. Campisi said. "But we
now know that there are processes that are driving
aging, and that those processes can be meddled with."

___________________________________________

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