60 citations
,
January 2007 in “Human Genetics” In this study, researchers found that while the SNP rs6152 is strongly associated with androgenetic alopecia, the GGN triplet repeat is not, suggesting the causative variant is likely a non-coding one.
71 citations
,
November 2005 in “The journal of investigative dermatology. Symposium proceedings/The Journal of investigative dermatology symposium proceedings” This review discusses the role of Edar signaling in hair follicle development and cycling, emphasizing its impact on cell fate, differentiation, and interactions with other pathways, but reports no new results.
195 citations
,
June 2005 in “American Journal of Human Genetics” Genetic variation in the androgen receptor gene mainly causes early-onset hair loss, with maternal inheritance playing a key role.
76 citations
,
April 2005 in “Cancer Epidemiology, Biomarkers & Prevention” This study found that the AR-E211 A allele is associated with a lower risk of both metastatic prostate cancer and androgenetic alopecia in an Australian population.
75 citations
,
January 2004 in “Molecular and Cellular Biology” In this study, EDA-A2 transgenic mice exhibited multifocal myodegeneration dependent on XEDAR, suggesting a potential role for XEDAR in skeletal muscle homeostasis.
299 citations
,
March 2001 in “Journal of Investigative Dermatology” This study found that specific genetic markers near the androgen receptor gene are significantly more common in men with male pattern baldness, suggesting a genetic component in its development.
169 citations
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June 1998 in “Journal of Investigative Dermatology” This study found no significant genetic association between the 5α-reductase enzyme genes and male pattern baldness, suggesting a polygenic etiology rather than simple inheritance.
203 citations
,
November 1984 in “Journal of the American Academy of Dermatology” This study presents evidence suggesting that androgenetic alopecia is most likely inherited through a polygenic model, challenging the traditional view that it is caused by a simple Mendelian autosomal dominant gene.