Androgenic alopecia: Recent understanding of the androgenetic receptor-mediated molecular mechanisms and current pharmacotherapy

Androgenic alopecia (AGA), also called male-pattern hair loss, is a hair loss condition facilitated by dihydrotestosterone (DHT), the potent form of testosterone. The hallmark of this disorder is a patterned decrease in scalp hair density. In androgenic alopecia, 5α-reductase iso-enzyme, which is responsible for conversion of testosterone to DHT, is increased in the scalp follicles. In the presence of DHT, hair cycle is shortened and progressively miniaturizes scalp follicles. Like most tissues, hair undergoes continuous turnover throughout life. Hair follicles are replaced periodically; the time interval is dependent on location and by the process of hair cycling. AGA occurs in a sequential step. In genetically predisposed men the initial development is bitemporal recession, followed by diffuse frontal loss and after there a bald patch over the vertex of the scalp accurse. Ultimately, all the hair over the crown is lost. With each new cycle, hair follicles are regenerated and follicular stem cells are responsible for this and recapitulate many of the signals of embryologic development. Various factors are influence and alter the regenerating hair follicle with advancing age. In this review, the recent advances in the understanding of molecular mechanisms of androgenic alopecia are discussed. The recent developments in the pharmacotherapy of this condition is also reviewed and presented.