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

## TL;DR

Androgenetic hair loss is influenced by multiple genes and biological pathways, with genetic risk varying across populations and between men and women.

## Contribution

The paper highlights recent genetic discoveries in androgenetic alopecia, emphasizing polygenic influences and the need for diverse and gender-specific studies.

## Key findings

- AGA is a polygenic disorder involving multiple pathways like androgen signaling and follicle development.
- Genetic risk varies across populations, with limited transferability of findings from European cohorts to other ancestries.
- Emerging data suggest distinct genetic risk factors in women compared to men.

## Abstract

Androgenetic hair loss is the most common cause of gradual hair thinning in adults. For many years, this form of hair loss was thought to be driven mainly by male hormones and inherited in a simple way. Recent genetic research has shown that hair loss is influenced by many genes that affect how hair follicles grow, survive, and respond to hormones. These genes act through several biological pathways, leading to progressive thinning of hair follicles over time. Genetic risk also differs between populations, meaning that results from one ancestry group may not apply equally to others. In women, the genetic factors involved in hair loss appear partly different from those in men, and more research focused on women is still needed. Studies are also beginning to show that a person’s genetic makeup may influence how well certain hair loss treatments work or whether side effects might occur. New methods that study individual cells in hair follicles are improving understanding of how genetic risk leads to hair thinning and may help guide more personalized treatments in the future.

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.