more saturated cellular membranes...more resistant to ROS
deuterated PUFAs
protein variants expressed by centenarians
This is all messing-with-metabolism. How are you going to slow metabolism in humans? Supposedly, hyaluronic acid is what keeps naked mole rats from developing cancer. Do you think it would be a good idea to start injecting people with that stuff? Also, none of those animals avoid aging. Centenarians still age and die. More saturated cellular membranes and deuterated PUFAs might be more resistant to ROS, but that will only slow aging at best, not reverse it. There’s just no reason to think that MWM could ever cure aging.
Protein traffic jams
isn’t mentioned by SENS and can occur even w/o protein aggregates or lipofuscin
Actually, they occur due to TDP-43 and FUS aggregates gumming up the nuclear transport system. The SENS solution is to get rid of this aggregate junk, of course. These specific aggregates aren’t mentioned by SENS, but they fit within the SENS damage category of “intracellular aggregates.”
mitochondrial transfer
as an alternative to mitoSENS
Yeah, but what happens to the mutant mitos?
And in any case, this can be considered a different approach to MitoSENS, not an alternative. Yet another approach is the Shift effect. MitoSENS isn’t wedded to the notion of copying non-mutated mito genes into the nucleus.
IPSCs and epigenetic/genetic reprogramming
iPSCs are useful for stuff like WILT and to replace cells that aren’t so easily replaced in organs like the brain.
Transient reprogramming is also potentially useful, but more research is needed to determine whether or not it could lead to cancer.
glycosylation
This seems more like age-related changes in glucose and hormone levels that should return to normal once the relevant damage is repaired, rather than something for SENS to target directly, but I’ll need to double check.
This is all messing-with-metabolism. How are you going to slow metabolism in humans? Supposedly, hyaluronic acid is what keeps naked mole rats from developing cancer. Do you think it would be a good idea to start injecting people with that stuff? Also, none of those animals avoid aging. Centenarians still age and die. More saturated cellular membranes and deuterated PUFAs might be more resistant to ROS, but that will only slow aging at best, not reverse it. There’s just no reason to think that MWM could ever cure aging.
Actually, they occur due to TDP-43 and FUS aggregates gumming up the nuclear transport system. The SENS solution is to get rid of this aggregate junk, of course. These specific aggregates aren’t mentioned by SENS, but they fit within the SENS damage category of “intracellular aggregates.”
Yeah, but what happens to the mutant mitos?
And in any case, this can be considered a different approach to MitoSENS, not an alternative. Yet another approach is the Shift effect. MitoSENS isn’t wedded to the notion of copying non-mutated mito genes into the nucleus.
iPSCs are useful for stuff like WILT and to replace cells that aren’t so easily replaced in organs like the brain.
Transient reprogramming is also potentially useful, but more research is needed to determine whether or not it could lead to cancer.
This seems more like age-related changes in glucose and hormone levels that should return to normal once the relevant damage is repaired, rather than something for SENS to target directly, but I’ll need to double check.