Background: Men and women can both experience the common type of hair loss known as androgenetic alopecia (AGA). Hair follicle miniaturisation is affected by a complicated interplay of inflammatory agents, hormones, and genetic predisposition. Advanced Glycation End Products (AGEs) and their receptors (RAGE) have been identified as putative participants in the pathophysiology of AGA, connecting inflammation and oxidative stress to changes in hair follicles. Objective: The purpose of this review is to investigate the relationship between AGA pathogenesis, RAGE production, and serum levels of AGEs. It explores the potential applications of AGEs and RAGE as diagnostic indicators or therapeutic targets, clarifying the molecular pathways by which they may affect follicular miniaturisation and hair loss. Conclusions: The pathogenesis of AGA is intricately linked to AGEs and RAGE, which may exacerbate oxidative stress and inflammation in the microenvironment of the hair follicle.