Aubrey de Grey on the Harvard Mouse News

On Facebook, Aubrey de Grey said:

Stari is right. Spectacularly oversold. The mice are broken in one very well-understood way (no telomerase, so eventually over-short telomeres), and they have been constructed so that that problem can be fixed with a drug, and lo, lots of the downstream consequences of the problem are also fixed. Duh.

Michael: the cancer issue is not really relevant here, no, because mice have lots of telomerase normally and don’t use telomerase thrift as an anti-cancer tactic.

Prior to that, I had said:

I’m surprised this happened so soon. Nothing like this has been achieved before. The lack of increased cancer risk is the key point.

Again, even if this is fixing something deliberately broken, I wasn’t aware of rejuvenation like this being achieved before. I must admit that in this field I generally just follow the popular science material and don’t delve too much into the literature, though. The only blog I really read that goes into the science is Fight Aging. Still, I’m waiting to hear of a prior example of rejuvenation on this scale being demonstrated as a proof of concept.

Comments

  1. Aubrey understandably doesn’t want to have to deal with the backlash in five years… “where’s my anti-aging pill you fraud?!”

    This is no cure for aging.

    That said, this is huge. We’ve never before seen an apparently old mammal grow younger.

    This is an very early proof on concept with (as Aubrey predicted) mice.

  2. Dave

    I don’t see how this gets us anywhere. You basically made mice exhibit aging-like symptoms by depriving them of a necessary enzyme, then gave it back to them and they felt better. But this doesn’t mean that giving them more than the normal amount of the enzyme will do any good.

    If they had given normal mice more of the telomerase, and those mice had actually gone backwards in aging, then we’d be cooking with gas.

  3. Mephistopheles

    “If they had given normal mice more of the telomerase, and those mice had actually gone backwards in aging, then we’d be cooking with gas.”

    Exactumundo. How I long for that day.

    Though as I understand it telomere biology between mice and humans is very different – as in more different than usual.

  4. It does get us places in terms of PR, I suppose, which can be important, though ultimately life-extension research is the most important.

  5. Kevin Perrott

    Rejuvenation of multiple systems, not just slowing down of degeneration ala caloric restriction, has never been done before, even in a poor model of aging. This is amazing and worthwhile, especially for the PR that may help generate more resources for more research aimed at interventions.

  6. Arnie Christianson

    I think it is telling that Aubrey’s group has shifted (or perhaps augmented is the right word) its focus a bit away from whole-organism life extension to individual system regeneration.

    If you haven’t done so, I would actually recommend reading Aubrey’s book, as he does a very good job of explaining the limitations of telomerase therapies.

    Personally, I think the ability to regenerate individual organs and systems would get us to longevity escape velocity faster than overall, whole-organism life-extension. The former is actually a means to the latter, and there have been and continue to be reportable successes in this area.

  7. If you’re not already familiar with it, you might want to check out longevitymeme.org for short blog post length updates on anti-aging that are fairly sciency.

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