4 ms·
I'm no biologist, but I think you're missing some causes of aging. DNA isn't the only thing that has to stay mutation free for an organism to not age. Lots of
by space_fountain 7y ago
I'm no biologist, but I think you're missing some causes of aging.
DNA isn't the only thing that has to stay mutation free for an organism to not age. Lots of the cellular machinery will propagate error to future generations. For a simple example see prion diseases. Sure they seem big scary and rare, but I'd suspect in reality this sort of thing happens way more often than we probably realize just in ways that can't be spread person to person even via cannibalism or that has much lower consequences.
Keep in mind also that ending aging is striving against not just entropy but evolution. Cancer cells are selected for. Obviously not on a species level, but if even just one cell messes and starts reproducing out of control it will quickly take over. You can implement more checks along the way and repair damage as it comes up, but the point remains that if even just one cell somehow isn't effected, it will be selected for among all the cells that make you up.
- The_rationalist 7y agoThank you for the feedback! DNA isn't the only thing that has to stay mutation free for an organism to not age. Could we draw a list? Your example on prion is incorrect as prion are misfolded proteins made by buggy DNA genes. https://en.m.wikipedia.org/wiki/Prion https://en.m.wikipedia.org/wiki/Prion Another thing that I identify as contributing to aging other than cell DNA is mitochondrial DNA (it's weird to realize we have two different DNA in each cells) Does other organelles apply? I fking don't know and how could I? :(
- COGlory 7y agoPrion pathophysiology isn't completely understood, and there's some literature to suggest certain types are caused by environmental factors. Regardless, curing cell aging is only the first step in "curing" aging. Some cell types simply stop dividing as a natural part of the lifecycle, and it isn't necessarily telomere related. Additionally, the only cells that don't shorten telomeres over time are cancer cells. Aging is a complicated process we don't understand.
- The_rationalist 7y agoSome cell types simply stop dividing as a natural part of the lifecycle https://en.m.wikipedia.org/wiki/Hayflick_limit https://en.m.wikipedia.org/wiki/Hayflick_limit It's because they have too much DNA damage. Aging is a complicated process we don't understand. I mostly disagree, while it is unknown how much of ageing is not a cause of DNA damage, I expect by far most of it come from DNA damage. Btw: are organelles just protein complexes? If so organelles are made by DNA too.
- COGlory 7y agoThe hayflick limit isn't the only cause of senescence. There are many biochemical processes that can induce senescence, and a variety of reasons the cell might do that. Oncogenic stress from reactive oxygen species, double stranded DNA breaks, enzymes like p53 tumor suppressor (this is a big one) and histone deacetylase inhibitors can all lead to senescence. Also, the hayflick limit has little to do with DNA damage per se, but rather is about telomere shortening. DNA is replicated in a ssomewhat asymmetrical fashion, and at the end of the chromosome, and needs the telomere to act as a buffer. Eventually you run out of buffer because every replication loses a little bit. But there's no innate damage to the DNA related to telomere shortening - all of the generic code still is maintained. >Btw: are organelles just protein complexes? If so organelles are made by DNA too. No... Not even close. There are some proteins in them and proteins interact with them but organelles are extremely complex. They are structures made of lipids, proteins, minerals, RNA, etc.