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I could not disagree more. As the article states, and this meshes with my layperson's understanding, mitochondrial malfunction is a key facet of aging. While we

I could not disagree more. As the article states, and this meshes with my layperson's understanding, mitochondrial malfunction is a key facet of aging. While we strongly suspected the role of mitochondria, being able to turn them on and off and observe their effect really cements our understanding that, yes, they are involved in the ways we think they are. Further cause for optimism is that toggling the mitochondria toggled other age-associated behaviors in the mice. One of the pillars of SENS is allotropic expression of a subset of mitochondrial genes in the nucleus, to get those genes away from the mitochondrial furnace. We can speculate that other mitochondrial gene therapies may emerge from work like this. I can't be disappointed by this progress!

TheSpiceIsLife 8y ago
In this context, is SENS Strategies for Engineered Negligible Senescence?
- theothermkn 8y ago
  Yup. I'm hopeful about the work associated with Aubrey de Grey and the SENS foundation. Again, this is from a layperson's perspective. My mind was kind of blown by the YouTube videos of the Undoing Aging 2018 conference, especially the speaker whose company is doing work on triggering apoptosis in senescent cells. It feels like things are starting to yield.
  - rsync 8y ago
    "triggering apoptosis in senescent cells" You can do this right now with very vigorous exercise. In fact, it appears that ones own mitochondrial population can be kept "young" by constantly weeding out cells with poor energy efficiency. Sort of a intra-body natural selection with exercise as the environmental stressor. There is a very interesting book by Nick Lane titled _Power, Sex, Suicide_ that explores these ideas. Not to worry, I suppose, since anyone with even a fleeting interest in "life extension" or "anti aging" would have a comprehensive, extremely intense exercise regimen ... Right ?
    - lowdest 8y ago
      > since anyone with even a fleeting interest in "life extension" or "anti aging" would have a comprehensive, extremely intense exercise regimen ... Right ? Absolutely. And my adherence to it is at least as fleeting.
reasonattlm 8y ago
No, this really is breaking the mice, not inducing something that looks like SENS-relevant damage in mitochondria. The details matter. Many means of breaking cell biology can produce things that look superficially like accelerated aging in at least some ways. That doesn't mean it is aging: given that aging is widespread tissue dysfunction, anything that causes widespread tissue dysfunction can have overlapping phenotypes, but that doesn't mean it has anything to do with normal aging. DNA repair deficiency is the usual example - something that isn't all that apparent in normal aging, in comparison to the models in which DNA repair machinery is missing or broken. So, similarly, pulling the rug out from under mitochondrial function can be done in countless ways that have very little to do with what happens in aging. I think the onus is still on these researchers to demonstrate that the method they have chosen has much of anything to do with aging per se.
- theothermkn 8y ago
  To me, this is akin to finding out what happens to airplanes when their pilots die. If we're wondering about this because they have been dying of asphyxiation at altitude, we'd still learn something if we ran the experiment of shooting them dead at altitude. The conditions aren't exactly the same, but we'll still figure out that pilots are important to airplanes. The other thing worth noting is that there could be some confusion from the title. It has "aging-associated" in it. The charitable understanding is along the lines of my analogy. The uncharitable, and seemingly popular one, is along the lines of your counterargument, and I think interprets "aging-associated" as "due to or consequent of aging," rather than "due to a cause that is similar on one level to causes that come about by aging."

TheSpiceIsLife 8y ago

In this context, is SENS Strategies for Engineered Negligible Senescence?

theothermkn 8y ago
Yup. I'm hopeful about the work associated with Aubrey de Grey and the SENS foundation. Again, this is from a layperson's perspective. My mind was kind of blown by the YouTube videos of the Undoing Aging 2018 conference, especially the speaker whose company is doing work on triggering apoptosis in senescent cells. It feels like things are starting to yield.
- rsync 8y ago
  "triggering apoptosis in senescent cells" You can do this right now with very vigorous exercise. In fact, it appears that ones own mitochondrial population can be kept "young" by constantly weeding out cells with poor energy efficiency. Sort of a intra-body natural selection with exercise as the environmental stressor. There is a very interesting book by Nick Lane titled _Power, Sex, Suicide_ that explores these ideas. Not to worry, I suppose, since anyone with even a fleeting interest in "life extension" or "anti aging" would have a comprehensive, extremely intense exercise regimen ... Right ?
  - lowdest 8y ago
    > since anyone with even a fleeting interest in "life extension" or "anti aging" would have a comprehensive, extremely intense exercise regimen ... Right ? Absolutely. And my adherence to it is at least as fleeting.

reasonattlm 8y ago

No, this really is breaking the mice, not inducing something that looks like SENS-relevant damage in mitochondria. The details matter. Many means of breaking cell biology can produce things that look superficially like accelerated aging in at least some ways. That doesn't mean it is aging: given that aging is widespread tissue dysfunction, anything that causes widespread tissue dysfunction can have overlapping phenotypes, but that doesn't mean it has anything to do with normal aging. DNA repair deficiency is the usual example - something that isn't all that apparent in normal aging, in comparison to the models in which DNA repair machinery is missing or broken. So, similarly, pulling the rug out from under mitochondrial function can be done in countless ways that have very little to do with what happens in aging. I think the onus is still on these researchers to demonstrate that the method they have chosen has much of anything to do with aging per se.

theothermkn 8y ago
To me, this is akin to finding out what happens to airplanes when their pilots die. If we're wondering about this because they have been dying of asphyxiation at altitude, we'd still learn something if we ran the experiment of shooting them dead at altitude. The conditions aren't exactly the same, but we'll still figure out that pilots are important to airplanes. The other thing worth noting is that there could be some confusion from the title. It has "aging-associated" in it. The charitable understanding is along the lines of my analogy. The uncharitable, and seemingly popular one, is along the lines of your counterargument, and I think interprets "aging-associated" as "due to or consequent of aging," rather than "due to a cause that is similar on one level to causes that come about by aging."