Slowing aging by purging senescent cells | Hacker News Reader

Slowing aging by purging senescent cells

nytimes.com

38 pointsunignorant10 comments

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...

"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...

Eh, innovative research in all fields of biomedicine is difficult to get funded. Hell, even super-safe run-of-the-mill research is difficult to get funded. There simply are not enough dollars to go around and it is only getting worse.

The NIH has taken the view that steady, incremental progress is a better use of money than swinging for the fences. While I'm not defending the NIH's decisions, I can understand the reasoning.

And regarding de Grey...well, I can appreciate his contribution to raising awareness. Otherwise, his views are somewhat akin to claiming "Like, what if we are living in the matrix, man?" as "Philosophy".

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.

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...

And heavy in depth commentary:

http://sens.org/node/2449

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...

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.

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

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

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.

Discussed on the Diane Rehm show on NPR today http://thedianerehmshow.org/shows/2011-11-22/new-development...

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).

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