Androgenetic Alopecia and Thyroid Cancer: Coincidence or More?

The document reviewed the genetic and molecular aspects of androgenetic alopecia (AGA), the most common form of hair loss affecting 80% of Caucasian men and 50% of Caucasian women. It highlighted the role of androgens and genetic predisposition in AGA, noting that the condition was associated with increased androgen receptor activity and 5-alpha reductase enzyme expression in affected scalp areas. Genome-wide association studies identified significant genetic loci, particularly on the X chromosome, implicating the androgen receptor (AR) and ectodysplasin A2 receptor (EDA2R) genes in AGA. The AR gene was estimated to confer up to 40% of the genetic risk for AGA. The review also discussed the role of follicle miniaturization, microinflammation, and the Wnt signaling pathway in AGA pathogenesis, suggesting that nonandrogen-dependent pathways might also be involved. Further research was needed to fully understand the molecular mechanisms underlying AGA. The study explored the genetic and molecular aspects of androgenetic alopecia, highlighting the miniaturization of hair follicles as a key feature. It identified differentially expressed genes in affected scalp regions and suggested that androgens play a crucial role by inhibiting Wnt/B-catenin and Notch signaling pathways, leading to follicle miniaturization. The overexpression of prostaglandin synthase (PGDS) and prostaglandin D2 (PGD2) was noted as a potential therapeutic target. The research emphasized the need for further studies on the epigenetic aspects of androgenetic alopecia, particularly the global methylation profile, to better understand its molecular pathophysiology.