Background: Androgenetic alopecia (AGA) is the most common form of non-scarring alopecia in humans. Several studies have used different laboratory models to study the pathogenesis and interventions for AGA. These study models have proved beneficial and have led to the approval of two drugs. However, the need to build on existing knowledge remains by examining the relevance of study models to the disease. Objective: We sought to appraise laboratory or pre-clinical models of AGA. Method: We searched through databases (PubMed, ScienceDirect, Web of Science, World CAT, Scopus and Google Scholar) for articles on AGArelated studies from 1942 to March 2019 with a focus on study models. Results: The search rendered 101 studies after screening and deduplication. Several studies (70) used in vitro models, mostly consisting of twodimensional monolayer cells for experiments involving the characterization of androgen and 5-alpha reductase (5AR) and inhibition thereof, the effects of dihydrotestosterone (DHT) and biomarker(s) of AGA. Twenty-seven studies used in vivo models of mice and monkeys to investigate DHT synthesis, the expression and inhibition of 5AR and hair growth. Only four studies used AGA-related or healthy excisional/punch biopsy explants as ex vivo models to study the action of 5AR inhibitors and AGA-associated genes. No study used three-dimensional [3-D] organoids or organotypic human skin culture models.
Conclusion:We recommend clinically relevant laboratory models like human or patient-derived 3-D organoids or organotypic skin in AGA-related studies. These models are closer to human scalp tissue and minimize the use of laboratory animals and could ultimately facilitate novel therapeutics.
| BACKGROUNDAndrogenetic alopecia (AGA) is the most common form of non-scarring hair loss in humans. [1][2][3] The prevalence of AGA varies between races and ethnicities. 1 This disparity is attributed to the different methods of measuring prevalence, making it difficult to compare studies. 1,2 Nonetheless, about 50% of men of European descent are affected by the age of 50 years; this proportion increases to 90% with age. 1,4,5 Furthermore, AGA is estimated to affect about 19% of women of European ancestry, while the prevalence and severity of AGA are considered low in Asian and African men. 1,4,6 In the early 1940s, Hamilton proved that genetic predisposition and male hormone stimulation are prerequisites in AGA development. 7 After this discovery, several AGA models were created to delineate the pathophysiology and evaluate the effectiveness of novel therapeutics using both laboratory (in vitro, in vivo and ex vivo) and non-laboratory models. These models,This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.