The Genetic Landscape of Androgenetic Alopecia: Current Knowledge and Future Perspectives

Androgenetic alopecia (AGA) is the most common cause of progressive hair thinning in adults and has traditionally been viewed as an androgen-driven inherited condition. Genomic research now demonstrates that AGA is a complex polygenic disorder involving multiple biological pathways, including androgen signaling, hair follicle development, cell survival, and extracellular matrix remodeling. Genome-wide association studies have identified numerous susceptibility loci, revealing that follicle miniaturization arises from interacting molecular mechanisms rather than a single pathogenic process. Genetic risk and predictive value vary across populations, with many loci identified in European cohorts showing limited transferability to other ancestries, highlighting the need for more diverse genetic studies. In women, genetic studies remain underpowered, and emerging data suggest partially distinct risk architecture compared with male AGA. Pharmacogenetic findings indicate that genetic variation may influence response to commonly used therapies, although no markers are currently validated for routine clinical use. Advances in single-cell and multi-omic approaches are improving understanding of how genetic risk translates into follicular dysfunction, supporting the development of more personalized and mechanism-based treatment strategies.