Hair loses its color with age due to a decline in activity of melanocyte pigment-producing cells, likely another symptom of the general fading of stem cell populations throughout the body. A recent paper adds evidence for that view:
Hair graying is one of the prototypical signs of human aging, but its mechanism is largely unknown. To elucidate the mechanism of hair graying, we investigated gene expression related to melanogenesis in human hair.
The key molecules in melanogenesis, microphthalmia-associated transcription factor-M (MITF-M), Sox10, Pax3, tyrosine related protein-1 (TRP-1), and tyrosinase, were absent or greatly reduced in the bulbs of white hair compared to black hair.
Melanocyte stem cells (MSCs) or melanocytes express markers for neural crest cells, Sox10, Pax3, and MITF-M. Taken together, our data suggest that hair graying is caused by defective migration of MSCs into the bulb area of hair.
Setting any given group of aging stem cells back to work by introducing appropriate biochemical signals - or cloning many more stem cells to reintroduce into the body - are very plausible projects for the decade ahead. Either could greatly improve the immediate situation, and the second strategy has already been demonstrated in heart therapies. I can envisage cloning and reintroduction of massive numbers of melanocytes as a clinical method to reverse hair graying in the late 2010s.
Risk of cancer is the challenge to all these attempts to put stem cells back to work in the aging body. That risk is why evolution has left us with stem cell populations that decline in old age, as damage to cells and biological systems is accumulating. Introducing cloned stem cells seems pretty safe, based on the evidence to date, but turning stem cells back on through the use of biochemical signals is much more of an unknown. This challenge will be overcome, but it's yet more of an incentive to address the fundamental issue of age-related biochemical damage rather than patching issues one by one.