As telomeres got shorter, patterns of gene expression became more elderly and the likelihood of the onset of diseases of old age increased, according to many scientific studies.

For instance, microglial cells in the brain that clean up amyloid beta plaque leading to Alzheimer’s disease fail when they become senescent.

 

If senescence in the microglial cells (derived from hematopoietic stem cells) could be prevented, then Alzheimer’s disease due to the onset of senility might also be prevented. Similarly, when the lining of the vascular endothelium becomes senescent, it becomes more adhesive to monocytes and more likely to develop atherosclerotic plaque leading to attacks or strokes.

So taking small  molecule telomerase activators effective at increasing the telomere length of components of the blood was a very good bet for effective life extension. Similarly, when dermal fibroblasts go senescent, they begin to attack the extracellular matrix, producing wrinkles.

 

This does not happen at once to all of the fibroblasts, but gradually in a way that produces more and more defects in the extracellular matrix behind wrinkles. Thus a telomerase activator effective on dermal fibroblasts should prevent observable signs of old age such as wrinkles.

 
https://joshmitteldorf.scienceblog.com/2014/03/21/a-one-man-experiment-in-radical-anti-aging/