Androgenetic alopecia.
Publication Year:
2025
PubMed ID:
41068174
Funding Grants:
Public Summary:
Androgenetic alopecia (AGA) is a condition of scalp hair growth characterized by progressive miniaturization of hair follicles and a reduction in the number of active follicles. In general, frontal, mid-scalp and crown hair follicles in postpubescent men and in postmenopausal women are susceptible to AGA. In rare cases, premenopausal women and prepubescent individuals are affected. In men, AGA is hypothesized to be caused by increased androgen signalling within susceptible hair follicles, altering the levels of locally produced signalling factors that sustain hair growth, whereas the molecular basis of AGA in women remains undetermined. AGA displays variability in its time of onset, severity and distribution patterns, and genome-wide association studies have uncovered more than 380 genomic loci associated with AGA, including genes involved in androgen and WNT pathways. Furthermore, epidemiological studies support substantial ancestral variation in AGA. Effective therapies for AGA include autologous transplantation of androgen-resistant occipital hair follicles, oral finasteride and topical minoxidil. Not all individuals with AGA respond to these therapies or comply with daily use of medicines, creating a need for new approaches. Emerging therapies for AGA include hair follicle-activating peptides, mRNA-containing liposomes, as well as bioengineering of new hair follicles. AGA has a negative socioemotional effect on affected individuals, and its prompt diagnosis and treatment can improve self-reported quality of life.
Scientific Abstract:
Androgenetic alopecia (AGA) is a condition of scalp hair growth characterized by progressive miniaturization of hair follicles and a reduction in the number of active follicles. In general, frontal, mid-scalp and crown hair follicles in postpubescent men and in postmenopausal women are susceptible to AGA. In rare cases, premenopausal women and prepubescent individuals are affected. In men, AGA is hypothesized to be caused by increased androgen signalling within susceptible hair follicles, altering the levels of locally produced signalling factors that sustain hair growth, whereas the molecular basis of AGA in women remains undetermined. AGA displays variability in its time of onset, severity and distribution patterns, and genome-wide association studies have uncovered more than 380 genomic loci associated with AGA, including genes involved in androgen and WNT pathways. Furthermore, epidemiological studies support substantial ancestral variation in AGA. Effective therapies for AGA include autologous transplantation of androgen-resistant occipital hair follicles, oral finasteride and topical minoxidil. Not all individuals with AGA respond to these therapies or comply with daily use of medicines, creating a need for new approaches. Emerging therapies for AGA include hair follicle-activating peptides, mRNA-containing liposomes, as well as bioengineering of new hair follicles. AGA has a negative socioemotional effect on affected individuals, and its prompt diagnosis and treatment can improve self-reported quality of life.