Genetic components of androgenetic alopecia : a biochemical study

Abstract

Androgenetic alopecia (AGA) is an extremely common condition in males, caused by increased androgen levels in hair follicles, causing progressive miniaturisation leading to loss of hair on the scalp. It is known to be a polygenic complex trait, however the exact mechanism of its pathogenicity is still unknown. A number of loci have been associated with AGA, however these only explain ~80% of the heritability of the condition. In the study, 2 genes associated with AGA, CRHR1 and GOLGB1, were studied through analysis of the biomarkers involved in the pathways affected by these genes. A sample size of 420 samples from the Maltese Acute Myocardial Infarction (MAMI) Study were used as the study population. The levels of each biomarker were compared in balding and non-balding individuals, using the Kruskal-Wallis test to establish if any differences between the two groups was significant. Increased cortisol levels and decreased NF-κB2, NF-κB-Iα, IL-1β and IFN-γ levels were associated with balding in people under 50 years of age. Increased levels of insulin, insulin resistance and SBG, while decreased DHEA-SO4 and free testosterone levels were observed in balding individuals with no age restrictions. The differences within these biomarkers may be indicative of how genetic changes in balding individuals affect the pathobiology of balding.