title: Investigation of four novel male androgenetic alopecia susceptibility loci: no association with female pattern hair loss.
abstract: Female pattern hair loss (FPHL) is a common hair loss disorder in women and has a complex mode of inheritance. The etiopathogenesis of FPHL is largely unknown; however, it is hypothesized that FPHL and male pattern baldness [androgenetic alopecia (AGA)] share common genetic susceptibility alleles. Our recent findings indicate that the major AGA locus, an X-chromosome region containing the androgen receptor and the ectodysplasin A2 receptor (EDA2R) genes, may represent a common genetic factor underlying both early-onset FPHL and AGA. This gives further support for the widespread assumption of shared susceptibility loci for FPHL and AGA. However, we could not demonstrate association of further AGA risk loci, including 20p11, 1p36.22, 2q37.3, 7p21.1, 7q11.22, 17q21.31, and 18q21.1, with FPHL. Interestingly, a recent study identified four novel AGA risk loci in chromosomal regions 2q35, 3q25.1, 5q33.3, and 12p12.1. In particular, the 2q35 locus and its gene WNT10A point to an as-yet unknown involvement of the WNT signaling pathway in AGA. We hypothesized that the novel loci and thus also the WNT signaling may have a role in the etiopathogenesis of FPHL and therefore examined the role of these novel AGA risk loci in our FPHL samples comprising 440 German and 145 UK affected patients, 500 German unselected controls (blood donors), and 179 UK supercontrols. Patients and controls were genotyped for the top two single nucleotide polymorphisms at each of the four AGA loci. However, none of the genotyped variants displayed any significant association. In conclusion, the results of this study provide no support for the hypothesis that the novel AGA loci influence susceptibility to FPHL.
authors.affiliation: Institute of Human Genetics, University of Bonn, Sigmund-Freud-Str. 25, 53127, Bonn, Germany.
authors.forename: Rima
authors.initials: R
authors.lastname: Nuwaihyd
authors.forename: Silke
authors.initials: S
authors.lastname: Redler
authors.forename: Stefanie
authors.initials: S
authors.lastname: Heilmann
authors.forename: Dmitriy
authors.initials: D
authors.lastname: Drichel
authors.forename: Sabrina
authors.initials: S
authors.lastname: Wolf
authors.forename: Pattie
authors.initials: P
authors.lastname: Birch
authors.forename: Kathy
authors.initials: K
authors.lastname: Dobson
authors.forename: Gerhard
authors.initials: G
authors.lastname: Lutz
authors.forename: Kathrin A
authors.initials: KA
authors.lastname: Giehl
authors.forename: Roland
authors.initials: R
authors.lastname: Kruse
authors.forename: Rachid
authors.initials: R
authors.lastname: Tazi-Ahnini
authors.forename: Sandra
authors.initials: S
authors.lastname: Hanneken
authors.forename: Markus
authors.initials: M
authors.lastname: Böhm
authors.forename: Anja
authors.initials: A
authors.lastname: Miesel
authors.forename: Tobias
authors.initials: T
authors.lastname: Fischer
authors.forename: Hans
authors.initials: H
authors.lastname: Wolff
authors.forename: Tim
authors.initials: T
authors.lastname: Becker
authors.forename: Natalie
authors.initials: N
authors.lastname: Garcia-Bartels
authors.forename: Ulrike
authors.initials: U
authors.lastname: Blume-Peytavi
authors.forename: Markus M
authors.initials: MM
authors.lastname: Nöthen
authors.forename: Andrew G
authors.initials: AG
authors.lastname: Messenger
authors.forename: Regina C
authors.initials: RC
authors.lastname: Betz
mesh_terms: D000505:Alopecia / Q000235:genetics*; D005260:Female; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide; D011944:Receptors, Androgen / Q000235:genetics*; D051153:Wnt Proteins / Q000235:genetics*; D060449:Wnt Signaling Pathway / Q000235:genetics; D053340:Xedar Receptor / Q000235:genetics*
chemical_list: C506011:EDA2R protein, human; D011944:Receptors, Androgen; C484142:WNT10A protein, human; D051153:Wnt Proteins; D053340:Xedar Receptor