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Loss of epigenetic information as a cause of mammalian aging

cell.com

21–30 of 57 posts

Re: Loss of epigenetic information as a cause of mammalian aging

#21

I think its a cool theory and seems the most reasonable from all the other theories of aging. However I am a bit disappointed when I only see David's name on every paper published on this topic. Why dont other institutions start similar studies to verify this claim?

All the top postdocs would rather work at the well-known lab with lots of grant money and experience.

I'm sure someone else is trying, but there's an agglomerative effect here, where a competing lab would be starting at a disadvantage and playing with a B-team.

Re: Loss of epigenetic information as a cause of mammalian aging

#24
It seems like it should be possible to build a drop-in replacement system for DNA that adds a more robust error detection/correction capability. Each gene gets a checksum at the end and the transcription/translation processes are amended to validate these prior to progressing to building proteins.

Obviously it would be more complex than just that but it would be interesting to see how it affects biology. Evolution would now be done primarily though gene mixing vs random mutation, it also seems that things like ionizing radiation could be much more directly harmful, but cancer and autoimmune diseases would seem to be substantially diminished.

No idea how it would affect aging. Seems like it would slow it down but I’m sure it’s more complicated than that.

Re: Loss of epigenetic information as a cause of mammalian aging

#25

Earlier quoted context omitted.

I assume the time to publish is too long, and the research too expensive. Aging takes time. Hopefully this changes soon.

Coming soon, on-demand aging.

YC 2043: Aging as a service. AaaS.

Re: Loss of epigenetic information as a cause of mammalian aging

#26
Interesting publication by Sinclair back in 2021: Reprogramming to recover youthful epigenetic information and restore vision

> Using the eye as a model CNS tissue, here we show that ectopic expression of Oct4 (also known as Pou5f1), Sox2 and Klf4 genes (OSK) in mouse retinal ganglion cells restores youthful DNA methylation patterns and transcriptomes, promotes axon regeneration after injury, and reverses vision loss in a mouse model of glaucoma and in aged mice.

[0] https://www.nature.com/articles/s41586-020-2975-4

Re: Loss of epigenetic information as a cause of mammalian aging

#27
post #3

What makes me somehow believe in the information theory of aging is that old people look "noisy".

Sure, but "ageing is a result of increasing entropy" is pretty much the same as saying that ageing is caused by the passage of time. The interesting part here is that they narrow down which loss of information is important.

Since humans eat food, they are not subject to entropy necessarily increasing over time (as long as food is available).

Re: Loss of epigenetic information as a cause of mammalian aging

#28
post #8

Earlier quoted context omitted.

Increasing entropy in a system can be avoided with an external energy source.

Well what you need is more like an easily accessible source of low entropy. You can substitute a big concentration of energy (the concentration part is important) to some extent. However the energy usage of a computer (the simplest example of a device that lowers entropy in a flexible way) is many orders of magnitude higher than the theoretical limit. So I'm not entirely sure how many bits of entropy it takes to reve…

Aging is reversed each time a zygote is made. No need for terajoules of energy.

Re: Loss of epigenetic information as a cause of mammalian aging

#30

> loss of epigenetic information is a reversible cause of aging Ok, so how do we reverse the loss of epigenetic information?

They use three of the four "Yamanaka factors," which are substances that, in combination, turn adult cells back into stem cells.
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