We get the usual story of how
this will take years. Try next year if
folks work out the many available pathways and jump on the protocol as they are
wont to do. The huge discovery here is
that age related diseases can be halted until you reach the maximum natural
lifespan of one hundred. Now I know how I
am going to reach the age of one hundred.
The good news is that this artificial increase is in living one’s life
in one’s prime is extended to the last days.
This actually happens in the wild for all creatures in the normal state
of nature.
Once this takes hold, pension
plans become irrelevant. Thus you can
avoid such schemes if you are presently in you twenties or even a lot older in
most cases. At least make sure there is
a good cash out arrangement.
Whatever is said about this it is
an excellent new protocol with direct therapeutic impact. Expect to take an age related series of doses
for about one year that is then followed with shorter programs every five years
or so. Also expect to be maintaining an
excellent level of safe fitness hereafter.
Removing Old Cells Could Extend Human Life
Jennifer Welsh, LiveScience Staff Writer
Date: 02 November 2011 Time: 02:00 PM ET
Removal of specific cells that accumulate with age can delay or prevent
the onset of age-related disorders, new research suggests. If adapted for
humans, this intervention may represent an avenue for treating or delaying
age-related diseases and improving healthy lifespan in humans.
CREDIT: Charles Shapiro, Dreamstime.com
The old adage "Out with the old and in with the new" could
help prevent age-related diseases if applied to certain cells, new research on
mice suggests.
By removing the body's worn-out cells, called senescent cells, several
times during the lifetime of aging-accelerated mice, researchers were
able to spare the mice of cataracts,aging
skin and muscle loss.
"We started treating animals when they were really young, before
they started to establish these senescent cells," study researcher Darren
Baker, of the Mayo Clinic College of Medicine in Minnesota, told LiveScience.
"As a cell became senescent we would remove it; we saw a really profound
effect."
Senescent cells
These cells were once important contributors to their cellular
community. Eventually cells get old and start showing signs of wear and tear
that could lead to cancer, so the body essentially "turns them off." When
cells get turned off in mammals (including humans and mice), they can take one
of two paths, either dying off or sticking around in a senescent state.
For some reason, the ones that stick around start pumping out odd
proteins. These chemical signals have a strange impact on the cells around
them, and researchers have speculated that these chemicals can lead to
age-related diseases.
The number of senescent cells increases
as tissues age; at most they will make up 15 percent of cells in mammalian
tissues, the researchers said.
Still, "that small percent is enough to cause major
consequences," Baker said. "They start to turn on a variety of genes
that are not good and are thought to be detrimental to the overall function of
the tissue."
Out with the old
In the new study, the team bred mice to age quickly, getting
cataracts, weakened muscles and loss of fat deposits by the time they are 10
months old, when they die of heart disease.
At the mice's 3-week birthdays, the researchers treated them with a
drug that would cause their senescent cells to commit suicide, and they
repeated this treatment every three days. Compared with the untreated mice that
kept all their senescent cells, these drug-treated mice had stronger
muscles, fewer
cataracts and less wrinkled skin (because their fat deposits in their
skin were in better shape).
The researchers also let some of these mice grow up, and didn't start
treating them until they were 5 months old. At this point the mice had already
developed aging diseases, including cataracts, and were suffering from muscle
and fat loss. The scientists weren't able to "undo" the aging that
had already occurred, but after repeated treatment to remove the senescent
cells, deterioration of the mouse muscles and fat cells stopped.
Healthy aging
The mice still had other age-related signs and didn't have an extended
lifetime; basically, the drug extended the proportion of "healthy
time" in their lives. The researchers said they believe death (and
these other aging diseases) is caused
through different pathways that aren't affected by these senescent cells.
They are repeating their study on normal mice, without the accelerated
aging mutation, but these studies will take years to complete, because normal
mice live so much longer (to about 3 years).
Since the study was performed using mice, the researchers still have a
long way to go before they reach a human therapy. The senescent cell-clearing
technique couldn't be used on humans, since it would require inserting a
special gene into human embryos, as was done with mice embryos.
However, Baker said the researchers could use the information they
gather from these mouse studies to develop
therapies for humans. Gene therapies could be used to target senescent
cells, or scientists could use a vaccine to train the human immune system to
attack these cells. Such therapies are far in the future, though, and still
require lots of basic science to back them up.
The study was published today (Nov. 2) in the journal Nature.
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