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Editorial recruitment of other neural regions in the processing of nonemotional stimuli in ADHD. Collectively, this is a promising time for research into the neurobiology of ADHD. Articles in this issue and elsewhere implicate NA DA dysregulation in the manifestation of symptoms and cognitive deficits associated with the disorder. Medications with demonstrable efficacy in the treatment of ADHD act mainly on these systems and have been shown to exert beneficial effects on aspects of cognition such as response inhibition ; in proof-of-concept studies. Translational approaches are shedding light on the precise neurochemical mechanisms. The body of evidence also implicates subtle structural and functional abnormalities of fronto-striatal-cerebellar circuitry in the manifestation of the disorder. Pharmaco-fMRI should be used in the future to investigate the effects of ADHD medications on neural activity during cognitive tests and to compare different agents. There is also a need for baseline factors influencing clinical outcomes to be explored. Specifically, it will be critical to examine whether baseline cognitive function and the presence of different genetic polymorphisms modulate treatment outcomes. It is hoped that research in these areas will contribute to the development of improved treatment algorithms for children and adults with ADHD, to reduce harms side effects and abuse potential ; and maximize clinical benefits. Samuel R. Chamberlain Trevor W. Robbins Barbara J. Sahakian Department of Psychiatry University of Cambridge School of Clinical Medicine Addenbrooke's Hospital Cambridge, United Kingdom Behavioural and Clinical Neuroscience Institute University of Cambridge Cambridge, United Kingdom This work was funded by a Grant from the Wellcome Trust 076274 Z 04 Z awarded to T.W. Robbins, B.J. Everitt, A.C. Roberts, and B.J. Sahakian ; . SRC was supported by a priority studentship from the Medical Research Council. TWR, BJS, and SRC consult for Cambridge Cognition. TWR consults for Eli Lilly. BJS has consulted for Shire and Novartis. We thank Natalia del Campo and Ulrich Muller for helpful feedback on this editorial.
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Introduction Osteoporosis is a widespread public health problem among postmenopausal women because of the association between low bone mass and the occurrence of vertebral and hip fractures.1 Bone mass is maintained locally by a balance between bone formation by osteoblasts and bone resorption by osteoclasts. Osteoblasts derived from mesenchymal tissues replace resorbed bone by elaborating matrix, which then becomes mineralized.2 After menopause, bone resorption exceeds bone formation. Consequent bone loss accompanied by an increased volume of adipose cells in bone marrow may inhibit osteoblast proliferation.3 Numerous factors, including bone morphogenetic protein-2 BMP2 ; , 4 transforming growth factor beta TGF-b ; , 5 and retinoic acid, 6 regulate osteoblastic bone formation. The secretion of many of these factors, including fatty acids, is affected during menopause. Previous studies have documented that dietary fat plays an important role in skeletal biology and bone health.7 Fatty acids may influence bone metabolism by altering the biosynthesis of prostaglandin PGE2 ; .810 In particular, n-3 polyunsaturated fatty acid PUFA.

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