That’s not the only thing that causes cytoskeleton damage.
Ultimately one path forward is: how do you create the data-set/papers that can be used by a new version of GPT-3 to suggest potential interventions for aging. That’s why ALL of the creative new technologies people use to treat genetic diseases or cancer (along with nanotechnology—yes UPenn people are already creating nanobots) can help, even if not originally designed for aging.
The point is that if the amount of tau/other junk could be kept low enough (by periodically removing it), then the accumulation of too much cytoskeleton damage should be avoided.
It’s not just tau/junk that contributes to cytoskeleton damage—the cytoskeleton is made of proteins that are easily oxidizeable in the same way that nuclear pore complexes are, and damage to NPCs don’t have tau as their primary culprit.
Too much tau junk → too much cytoskeleton damage
Too much lipofuscin/A2E → AMD
That’s LEV’s job (SENS 2, 3, etc.).
If you still think that there’s any potential primary damage targets that SENS doesn’t specifically mention, please let me know.
That’s not the only thing that causes cytoskeleton damage.
Ultimately one path forward is: how do you create the data-set/papers that can be used by a new version of GPT-3 to suggest potential interventions for aging. That’s why ALL of the creative new technologies people use to treat genetic diseases or cancer (along with nanotechnology—yes UPenn people are already creating nanobots) can help, even if not originally designed for aging.
The point is that if the amount of tau/other junk could be kept low enough (by periodically removing it), then the accumulation of too much cytoskeleton damage should be avoided.
It’s not just tau/junk that contributes to cytoskeleton damage—the cytoskeleton is made of proteins that are easily oxidizeable in the same way that nuclear pore complexes are, and damage to NPCs don’t have tau as their primary culprit.
Mutant mitochondria.