Journal
FRONTIERS IN NEUROENDOCRINOLOGY
Volume 35, Issue 3, Pages 331-346Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2014.03.003
Keywords
Autism; Basal ganglia; Imprinted gene; Mouse; Rat; Sex chromosome; Sry; Steroid sulfatase; Testosterone; Thalamus
Categories
Funding
- Medical Research Council [MR/L010305/1] Funding Source: Medline
- Medical Research Council [MR/L010305/1] Funding Source: researchfish
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Attention Deficit Hyperactivity Disorder (ADHD) is a developmental condition characterised by severe inattention, pathological impulsivity and hyperactivity; it is relatively common affecting up to 6% of children, and is associated with a risk of long-term adverse educational and social consequences. Males are considerably more likely to be diagnosed with ADHD than females; the course of the disorder and its associated co-morbidities also appear to be sensitive to sex. Here, I discuss fundamental biological (genetic and endocrine) mechanisms that have been shown to, or could theoretically, contribute towards these sexually dimorphic phenomena. Greater understanding of how and why the sexes differ with respect to ADHD vulnerability should allow us to identify and characterise novel protective and risk factors for the disorder, and should ultimately facilitate improved diagnosis, prognosis and treatment. (C) 2014 Elsevier Inc. All rights reserved.
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