5 ms·

Uh huh. I would like to have 3 questions answered: 1. How can the telomere shortening be reversed in an adult without inducing abberant cell growth? 2. How d

Uh huh. I would like to have 3 questions answered: 1. How can the telomere shortening be reversed in an adult without inducing abberant cell growth? 2. How do we stop stem cell populations from reaching senescence? 3. How do we deal with the fact that continued mitosis leads to an accumulation of copy-errors in aforementioned cell populations?

qaq 5y ago
Hyperbaric Oxygen Therapy (HBOT)?
nosianu 5y ago
To 1, telomeres; I need an expert to confirm or deny: I think to remember having read that the telomeres aren't really an issue. That that they get shorter is a consequence, not a reason - they are not needed because death of the cell occurs earlier. I also think to remember there actually is a mechanism (a protein) to extend them, it's just that in places where it wasn't needed it is not used and evolution therefore removed it, because it had no consequence. I think it was form one of the books of (biochemist) Nick Lane. Myself, I only took the basic bio-chem course so I never got to such advanced specialized topics. EDIT: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933587/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933587/ > 1. Do telomere biology and telomerase activity determine aging? > The first aspect to this question is whether differences in aging rates among mammalian species are caused in whole or in part by species-specific differences in telomerase/telomere biology. A very brief consideration of this question will show that this is unlikely. > There is little evidence that commonly observed changes in older individuals, such as anemia and impaired wound healing, result from impaired cellular proliferation, which would be the anticipated consequence of shortened telomeres (ofc there is a lot more details to consider)
- kettleballroll 5y ago
  It's been some time since I've worked in biology, but: telomere shortening is mostly a protection against aberant growth (ie, cancer): it sets an upper limit to how often a cell can multiply. If we'd live long enough that even healthy cells run up against that limit, we'd have to deactivate/reverse that mechanism. But then we'd lose one very effective defense against cancer.
  - subroutine 5y ago
    The mystery is that cell division isn't an issue for germline cells, like SSC, which replicate many times during your lifespan, and then keep on replicating during lifespans of all your progeny. https://en.wikipedia.org/wiki/Spermatogonial_stem_cell https://en.wikipedia.org/wiki/Spermatogonial_stem_cell That our germline cells are immortal, yet we are not, suggests that we (our bodies) are merely a replication vessel. Humans don't live to be 150 because (according to natural selection pressures) it's easier to just make a new version of you (or several) than to waste DNA space on efforts to keep 100-year-olds alive. The genome only serves the host through child-bearing years (plus a few extra bc grandma may still be useful to the survival of her grandchildren; what happens to grandma after 90 years old the germline cares not.
  - LinuxBender 5y ago
    There are some other compensating controls that can mitigate cancer but it takes some willpower which I suppose is an entirely different topic all together. This video [1] is worth a watch to learn a bit more about cancer as a metabolic disease. [1] - https://www.youtube.com/watch?v=06e-PwhmSq8 https://www.youtube.com/watch?v=06e-PwhmSq8 [video]
ben_w 5y ago
2. https://www.japantimes.co.jp/news/2021/12/12/national/science-health/aging-vaccine/ https://www.japantimes.co.jp/news/2021/12/12/national/scienc...

qaq 5y ago

Hyperbaric Oxygen Therapy (HBOT)?

nosianu 5y ago

To 1, telomeres; I need an expert to confirm or deny: I think to remember having read that the telomeres aren't really an issue. That that they get shorter is a consequence, not a reason - they are not needed because death of the cell occurs earlier. I also think to remember there actually is a mechanism (a protein) to extend them, it's just that in places where it wasn't needed it is not used and evolution therefore removed it, because it had no consequence. I think it was form one of the books of (biochemist) Nick Lane. Myself, I only took the basic bio-chem course so I never got to such advanced specialized topics. EDIT: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933587/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933587/ > 1. Do telomere biology and telomerase activity determine aging? > The first aspect to this question is whether differences in aging rates among mammalian species are caused in whole or in part by species-specific differences in telomerase/telomere biology. A very brief consideration of this question will show that this is unlikely. > There is little evidence that commonly observed changes in older individuals, such as anemia and impaired wound healing, result from impaired cellular proliferation, which would be the anticipated consequence of shortened telomeres (ofc there is a lot more details to consider)

kettleballroll 5y ago
It's been some time since I've worked in biology, but: telomere shortening is mostly a protection against aberant growth (ie, cancer): it sets an upper limit to how often a cell can multiply. If we'd live long enough that even healthy cells run up against that limit, we'd have to deactivate/reverse that mechanism. But then we'd lose one very effective defense against cancer.
- subroutine 5y ago
  The mystery is that cell division isn't an issue for germline cells, like SSC, which replicate many times during your lifespan, and then keep on replicating during lifespans of all your progeny. https://en.wikipedia.org/wiki/Spermatogonial_stem_cell https://en.wikipedia.org/wiki/Spermatogonial_stem_cell That our germline cells are immortal, yet we are not, suggests that we (our bodies) are merely a replication vessel. Humans don't live to be 150 because (according to natural selection pressures) it's easier to just make a new version of you (or several) than to waste DNA space on efforts to keep 100-year-olds alive. The genome only serves the host through child-bearing years (plus a few extra bc grandma may still be useful to the survival of her grandchildren; what happens to grandma after 90 years old the germline cares not.
- LinuxBender 5y ago
  There are some other compensating controls that can mitigate cancer but it takes some willpower which I suppose is an entirely different topic all together. This video [1] is worth a watch to learn a bit more about cancer as a metabolic disease. [1] - https://www.youtube.com/watch?v=06e-PwhmSq8 https://www.youtube.com/watch?v=06e-PwhmSq8 [video]

ben_w 5y ago

2. https://www.japantimes.co.jp/news/2021/12/12/national/science-health/aging-vaccine/ https://www.japantimes.co.jp/news/2021/12/12/national/scienc...