If you click the link to the actual paper, you’ll find:
> Next, we sought to explore the potential benefit of targeting the age-related increase of FTL1 in the hippocampus of aged mice. We performed targeted stereotaxic injections of a high-titer virus encoding shRNA sequences targeting either Ftl1 or luciferase control into the CA1 and dentate gyrus hippocampal regions of aged mice (Fig. 3b and Extended Data Fig. 5a,b).
There are lots of bio research techniques that can be applied to mice that you wouldn’t necessarily want to do to yourself…
In mouse by artificially increasing it. I guess there are lots of proteins that do this when at higher than normal levels.
This says nothing about the effects of artificially reducing levels in humans.
The article neglects to say HOW they "reduced FTL1."
If you click the link to the actual paper, you’ll find:
> Next, we sought to explore the potential benefit of targeting the age-related increase of FTL1 in the hippocampus of aged mice. We performed targeted stereotaxic injections of a high-titer virus encoding shRNA sequences targeting either Ftl1 or luciferase control into the CA1 and dentate gyrus hippocampal regions of aged mice (Fig. 3b and Extended Data Fig. 5a,b).
There are lots of bio research techniques that can be applied to mice that you wouldn’t necessarily want to do to yourself…
Also focusing on memory and metabolism, I thought it’s about aging in general such as muscles and mobility
Claude reckons by combatting spare iron in the blood (ftl1 is apparently iron-based), so iron chelators like green tea after every meal.