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Association of the steroid sulfatase ( STS ) gene with attention deficit hyperactivity disorder
Author(s) -
Brookes K.J.,
Hawi Z.,
Kirley A.,
Barry E.,
Gill M.,
Kent L.
Publication year - 2008
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30873
Subject(s) - attention deficit hyperactivity disorder , neuroactive steroid , steroid sulfatase , proband , genetics , single nucleotide polymorphism , major depressive disorder , candidate gene , gene , psychiatry , psychology , genotype , medicine , biology , mutation , steroid , mood , receptor , hormone , gabaa receptor
Abstract Attention deficit hyperactivity disorder (ADHD) is the most common behavioral disorder affecting children worldwide. The male bias in the prevalence of the disorder, suggests that some susceptibility genes may lie on the X chromosome. In this study we present evidence for a role of the X‐linked steroid sulfatase ( STS ) gene and neurosteroids in the development of ADHD. Previously it has been observed that probands with ADHD have lower serum concentrations of the neurosteroids DHEA, which is synthesized from DHEA‐S by STS . In further support, boys that suffer from XLI, a skin disorder caused by the deletion of the STS gene, have higher rates of ADHD, in particular the inattentive subtype. In a moderately sized sample of ADHD families (N = 384), we genotyped seven single nucleotide polymorphisms, tagging the entire gene. TDT analysis of the data yielded two polymorphisms that were significantly associated with ADHD (rs2770112—Transmitted: 71 Not Transmitted; 48; rs12861247—Transmitted: 43 Not Transmitted: 21), located towards the 5′ end of the gene ( P < 0.05). We conclude that the STS gene may play a role in susceptibility for ADHD, and that the neurosteroids pathways should be investigated further to access their potential contribution in susceptibility to the disorder. © 2008 Wiley‐Liss, Inc.