Rapamycin, telomeres, and the brain

It’s unfortunate that telomere lengths were overhyped in terms of longevity to the point that we threw the baby out with the bath water.
This shows the interdependence of rapamycin and TERT on brain mitochondrial function and aging.

In summary, 1. rapamycin reduces mitochondrial ROS and DNA damage in the brain and this action may be responsible for the improvement in brain function seen in both DR and rapamycin studies, even in the absence of structural changes.
2. Rapamycin is dependent upon mitochondrial TERT to exert its beneficial effects.
3. Rapamycin selectively translocates TERT from the nucleus of the neuron to the mitochondria which then allows for the rapamycin benefits.

Furthermore, recent studies along these lines suggest a role of immune cells, specifically Tregs, for the preservation of the brain and protection against neurodegeneration.

The significance of these findings regarding rapamycin and brain preservation could be extremely important.