I have specific ideas about why it will fail: the various interventions to combat the 7 damage types will all meet with complications and unexpected difficulties.
WILT, for example, might kill people or animals for years and years whilst the bugs are ironed out because they won’t get the cell replacement therapy right.
MitoSENS will unearth the complexities of mitochondrial DNA and why it’s hard to move it into the nucleus.
etc, etc.
But as we do this work, we will learn a lot about the body and there will be some amazing spinoffs. For example LysoSENS and AmyloSENS will probably help with age related diseases. Eventually it might even come together to extend lifespan for another 50 years until the next unforseen problem crops up. But I expect that to take at least till 2090, and a lot will have changed by then. By 2090, cryo, AI and uploading will probably look a lot better than being the next human lab-rat for SENS.
WILT, for example, might kill people or animals for years and years whilst the bugs are ironed out because they won’t get the cell replacement therapy right.
‘Ironing out’ is an understatement… how the heck do you get fingernail stem cells into the right spots and replenish every hair follicle? Bone marrow is easy, those cells move through the blood and colonize their proper niches when they flow through the bone. But solid tissue, with immobilized cells and extracellular matrix?
MitoSENS will unearth the complexities of mitochondrial DNA and why it’s hard to move it into the nucleus.
Oh hell yes. The animal mitochondrion is a crazy jerry-rigged mess with a genome more overoptimized than many viruses, bizarre specialized ribososomes specifically optimized for making the handful of proteins that the mitochondrial genome codes for while at the same time being obviously slapped together from spare parts, RNA-editing that sometimes is unclear what is important and what is noise, and some of the genes may need to be in the mitochondrion for the purpose of real-time regulation. And the same core set of genes coding for large, hydrophobic, membrane-bound proteins have failed to move into the nuclear genome in all branches of life because that stuff is damn hard to get through two membranes without having it congeal into pellets of inert goo. I’ve seen interesting work of late involving trying to get RNA-channels embedded in mitochondrial membranes to allow cytosolic RNAs with the proper signal sequences to get into the mitochondrion to be translated there, with some success, but I have little reason to think that such a system would improve upon normal mitochondrial function because poking a complicated system will often just make it worse. This is not to say that mitochondria are perfect, you can imagine in five seconds about twenty ways to make them better than they are—none of which are things you can do by simply going in and making a few simple mods to an existing eukaryotic system.
On another note it is pretty well impossible to get in and modify large fractions of cells in a living organism as opposed to a monolayer of cells in a controlled environment in a laboratory. This being said, I think one of the most fruitful avenues for actual anti-aging research would be looking for ways to chemically boost protein chaperone/recycling activity and improve the regulatory interactions between mitochondria and the cytosol.
I have specific ideas about why it will fail: the various interventions to combat the 7 damage types will all meet with complications and unexpected difficulties.
WILT, for example, might kill people or animals for years and years whilst the bugs are ironed out because they won’t get the cell replacement therapy right.
MitoSENS will unearth the complexities of mitochondrial DNA and why it’s hard to move it into the nucleus.
etc, etc.
But as we do this work, we will learn a lot about the body and there will be some amazing spinoffs. For example LysoSENS and AmyloSENS will probably help with age related diseases. Eventually it might even come together to extend lifespan for another 50 years until the next unforseen problem crops up. But I expect that to take at least till 2090, and a lot will have changed by then. By 2090, cryo, AI and uploading will probably look a lot better than being the next human lab-rat for SENS.
‘Ironing out’ is an understatement… how the heck do you get fingernail stem cells into the right spots and replenish every hair follicle? Bone marrow is easy, those cells move through the blood and colonize their proper niches when they flow through the bone. But solid tissue, with immobilized cells and extracellular matrix?
Oh hell yes. The animal mitochondrion is a crazy jerry-rigged mess with a genome more overoptimized than many viruses, bizarre specialized ribososomes specifically optimized for making the handful of proteins that the mitochondrial genome codes for while at the same time being obviously slapped together from spare parts, RNA-editing that sometimes is unclear what is important and what is noise, and some of the genes may need to be in the mitochondrion for the purpose of real-time regulation. And the same core set of genes coding for large, hydrophobic, membrane-bound proteins have failed to move into the nuclear genome in all branches of life because that stuff is damn hard to get through two membranes without having it congeal into pellets of inert goo. I’ve seen interesting work of late involving trying to get RNA-channels embedded in mitochondrial membranes to allow cytosolic RNAs with the proper signal sequences to get into the mitochondrion to be translated there, with some success, but I have little reason to think that such a system would improve upon normal mitochondrial function because poking a complicated system will often just make it worse. This is not to say that mitochondria are perfect, you can imagine in five seconds about twenty ways to make them better than they are—none of which are things you can do by simply going in and making a few simple mods to an existing eukaryotic system.
On another note it is pretty well impossible to get in and modify large fractions of cells in a living organism as opposed to a monolayer of cells in a controlled environment in a laboratory. This being said, I think one of the most fruitful avenues for actual anti-aging research would be looking for ways to chemically boost protein chaperone/recycling activity and improve the regulatory interactions between mitochondria and the cytosol.
“because poking a complicated system will often just make it worse.”
yeah that was my view. I have only an amateur interest in biology though.