Researchers at New York University’s Grossman School of Medicine published findings in the journal Nature detailing a mechanism linking hair graying to the physical stagnation of melanocyte stem cells (McSCs). The study, utilizing mice models, demonstrated that McSCs must travel between distinct compartments within the hair follicle to mature and produce the necessary pigment for hair color.
In a healthy state, these McSCs shuttle between the germ compartment, where WNT proteins promote regeneration, and other areas, allowing them to maintain their pigment-producing capability over time. However, the research indicated that as the hair regrowth process ages, McSCs frequently become lodged in the follicle bulge compartment, preventing their return to the germ compartment.
This fixed positioning effectively halts the production of melanin, resulting in hair growing without color, which manifests as gray hair. Mayumi Ito, the study's senior investigator, stated that this loss of "chameleon-like function" in the McSCs appears central to hair color loss.
The McSCs responsible for pigment are distinct from the cells that drive hair growth, meaning hair can continue to grow even after pigment production ceases. The NYU team observed that in older samples, nearly fifty percent of all McSCs could be found lodged in the non-pigment-producing bulge compartment.
Qi Sun, a postdoctoral fellow on the project, noted that these findings raise the possibility that the same mechanism of fixed positioning occurs in human subjects. If confirmed, this presents a tangible pathway for intervention focused on freeing these jammed cells to resume their function.
The researchers are now focusing on determining methods to restore motility to the McSCs once they become lodged. Successfully prompting these cells to move again could theoretically restart pigment creation, addressing the root cause of age-related hair graying.
While unrelated Harvard research suggests stress accelerates the aging pattern of hair follicles, this NYU study isolates a specific cellular mechanism for the loss of color itself. The failure of the McSC system appears to occur earlier than other adult stem cell populations in both mice and humans.
