

Slowing aging by purging senescent cells - unignorant
http://www.nytimes.com/2011/11/22/science/in-bodys-shield-against-cancer-a-culprit-in-aging-may-lurk.html?_r=1&src=dayp&pagewanted=all

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reasonattlm
This research is actually a good example of the profound institutional
problems with funding of aging and longevity science. Peter Thiel's call for
radical philanthropy addresses this issue - that funding has become staid, and
there needs to be more high-risk, high reward research funding akin to the
venture industry. See:

[http://www.fightaging.org/archives/2011/11/the-need-for-
visi...](http://www.fightaging.org/archives/2011/11/the-need-for-visionary-
philanthopy-in-longevity-science.php)

"So after Mayo Clinic researchers discovered they could delay degeneration of
the tissues in a fast-aging strain of mice by purging senescent cells, they
applied to the agency's National Institute on Aging for financing for the next
essential step, that of repeating the test in mice with a normal life span.
Under the agency's peer review system, panels of fellow experts judge each
proposal and assign it a score. On paper, it's hard to think of a better
system. But in practice, experts often differ, even on the best proposals, and
a single dissenting vote can reduce a proposal's overall score too low to get
financed. The Mayo proposal got a less than perfect score, and was denied
money. ... Their peer review process is not promoting innovative, high-risk
research. ... They were able to get their research started only because
private funds were available from the Ellison Medical Foundation, supported by
Larry Ellison of the Oracle software company, and from Robert P. Kogod, a
philanthropist in Washington. After publication of the Mayo Clinic team's
paper in Nature this month, they were approached by the Glenn Foundation, set
up by the commodities trader Paul F. Glenn, who has a longstanding interest in
aging research. The foundation gave them an unsolicited $60,000 and said it
would be around to talk later."

You'll recognize a number of those names as supporters of the SENS Foundation
and Methuselah Foundation before it over the past four or five years, having
put millions of dollars collectively into the work of those organizations on
(a) the basis for rejuvenation biotechnology and (b) what might charitably be
looked on as kicking the research community in the pants to make them get on
and do the damn job and make some noise about it.

In fact wherever there is somewhat innovative research into aging and
longevity - looking at repair, not just trying to find drugs to replicate the
effects of calorie restriction and push through the same old tired FDA
processes - you'll see many of the same visionary philanthropists behind the
scenes.

A related item by Aubrey de Grey on why people with the means are not pumping
as much funding as they can into longevity science, given the clear and
amazing payoffs:

[http://hplusmagazine.com/2011/11/21/why-arent-more-
wealthy-p...](http://hplusmagazine.com/2011/11/21/why-arent-more-wealthy-
people-funding-aging-research/)

~~~
jerf
There's also the possibility is that this is less deserving of study than you
may think. If this is the paper I saw a couple of weeks ago, they built mice
that die rapidly of a thing that mimics old age senescence by causing cells to
die of something that appears to be old age, then demonstrate that by flushing
out these artificially aged cells, which they accomplished via picking these
cells out with a tag they created in the first place, they can get back to the
mice's original life span without these modifications. As legitimately
interesting as this is from a research and learning point of view, I do not
think it is at all clear that this is actually going to lead to a therapy that
works on animals that haven't been artificially manipulated to produce this
particular problem.

The press releases make this sound like the sort of research that should be
shot to the top of all priorities, but when you really examine it, that
assessment doesn't hold up very well. It may still be important, but it isn't
as important as the news articles make it sound. The less-than-perfect grading
is probably correct.

Now, had they demonstrated mice that lived _longer_ than the core breed after
this treatment, I'd be singing a different song.

~~~
reasonattlm
This is actually one of the more important pieces of foundational work in the
last year in longevity science; it validates a great deal of other work and
theory on the role of senescent cells, and provides a working method of
eliminating senescent cells, which had been lacking until now. See commentary:

[http://www.fightaging.org/archives/2011/11/a-demonstration-o...](http://www.fightaging.org/archives/2011/11/a-demonstration-
of-the-merits-of-apoptosens.php)

And heavy in depth commentary:

<http://sens.org/node/2449>

------
adrianwaj
Cell death: you're fired, pack your stuff, it's too risky for you to stay

Cell senescence: stay, but your contract won't be renewed

I wonder if it's possible to reactivate a senescent cell by repairing the
damage that triggered it in the first place: repair and rejuvenation.

Add: possibly no: "repair to DNA normally take place during DNA replication
when cells are dividing, but post-mitotic cells do not divide. The main
concern in this instance is not whether there is a decrease in the ability of
cells to repair DNA with age, but instead whether post-mitotic cells can
themselves repair DNA, if at all they need to"

[http://ageing-research.blogspot.com/2008/01/post-mitotic-
tis...](http://ageing-research.blogspot.com/2008/01/post-mitotic-
tissue_21.html)

Also, is it possible to replace a cell that has already suicided by causing an
improvement in conditions that'd ensure a replacement cell isn't tagged with
the same fate: reconditioning and recruitment.

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skmurphy
I wonder if low dose radation or low dose toxins that foster hormesis are
actually killing off these senescent cells.

~~~
codex
Other candidates: fasting, exercise, and low carb diets.

~~~
skmurphy
all of these are also good for you, but the senescent cell model was the first
one to suggest a mechanism of action for hormesis to me.

------
celias
Discussed on the Diane Rehm show on NPR today
[http://thedianerehmshow.org/shows/2011-11-22/new-
development...](http://thedianerehmshow.org/shows/2011-11-22/new-developments-
aging-research)

------
itmag
What kind of skills/training are necessary to do research on stuff like this?

I can imagine few things that are more worthwhile (and probably stimulating to
work on as well).

