I've been doing some literature research on the genetics of baldness. Yes, I'm trying to work out what we can say about Neandertal phenotypes, if you're wondering. I share part of my androgen receptor gene with the Vindija Neandertals, and so I'm interested.
Anyway, I was reading today a new paper that suggests the involvement of prostaglandin D2 in male pattern hair loss [1]. The paper gives a good, dense account of what is known about the mechanism:
In AGA, large “terminal” hair follicles forming thick hair shafts miniaturize over time to small follicles that generate microscopic effete hairs (8). Follicle miniaturization is accompanied by a decrease in the duration of the growing phase of the follicle (anagen), which normally lasts several years to produce hair more than 1 m long, but which decreases to only days or weeks in AGA. This results in an increase in the percentage of resting (telogen) hair follicles containing microscopic hairs in bald scalp (4). In addition to these intrinsic changes to the hair follicle, infiltrating lymphocytes and mast cells have been identified around the miniaturizing follicle (9), especially in the area of the stem cell–rich bulge area (10). Sebaceous glands, which attach to each follicle, hypertrophy in bald scalp (8). In balding scalp, the number of hair follicle stem cells remains intact, whereas the number of more actively proliferating progenitor cells markedly decreases (11). This suggests that balding scalp either lacks an activator or has an inhibitor of hair follicle growth.
The paper itself focuses on the molecular mechanism at work in a mouse model, and does not examine the genetics of risk within human samples. So no targets for me to look at yet. But the role of prostaglandins in sex development might have something to do with the reason male pattern baldness is such a common polymorphism in human populations worldwide.