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Volume 49, Issue 4, Pages 368-377 (April 2010)


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Familial Clustering and DRD4 Effects on Electroencephalogram Measures in Multiplex Families With Attention Deficit/Hyperactivity Disorder

Sandra K. Loo, Ph.D.aCorresponding Author Informationemail address, T. Sigi Hale, Ph.D.a, Grant Hanada, B.S.a, James Macion, B.A.a, Anshu Shrestha, M.P.H.a, James J. McGough, M.D.a, James T. McCracken, M.D.a, Stanley Nelson, M.D.b, Susan L. Smalley, Ph.D.a

Accepted 19 January 2010. published online 08 March 2010.

Objective

The current study tests electroencephalogram (EEG) measures as a potential endophenotype for attention deficit/hyperactivity disorder (ADHD) by examining sibling and parent–offspring similarity, familial clustering with the disorder, and association with the dopamine receptor D4 (DRD4) candidate gene.

Method

The sample consists of 531 participants (191 parents and 340 children) from 132 multiplex families with ADHD who participated in a larger genetics study. All members of the families underwent extensive assessment including semi-structured diagnostic interviews and EEG recording.

Results

Strong sibling similarity and parent–offspring correlations in EEG power emerged, suggesting high trait heritability. Increased theta power was observed among children with ADHD when compared with unaffected children, and there were no differences according to ADHD subtype. Within the parent sample, ADHD diagnostic status and ADHD subtype group differences emerged in the theta, alpha, and beta frequency bands. DRD4 effects for both parents and children were apparent in the beta frequency band and for children only in the theta frequency band.

Conclusions

This study suggests that EEG measures are a promising avenue of study in the search for putative endophenotypes for ADHD, and that variability at the DRD4 gene may contribute to this endophenotype.

a Semel Institute for Neuroscience and Human Behavior and David Geffen School of Medicine at the University of California, Los Angeles

b Department of Human Genetics at the University of California, Los Angeles

Corresponding Author InformationCorrespondence to: Dr. Loo, UCLA Semel Institute, Room 47-406, 760 Westwood Plaza, Los Angeles, CA 90095

 This work was supported by grants from the National Institute of Child Health and Human Development (CD40275 to S.K.L.), the National Institutes of Neurological Disease and Stroke (NS054124 to S.K.L.) and National Institutes of Mental Health (MH058277 to S.L.S.).

 Disclosures: Dr. McGough consults and receives research support from Eli Lilly & Company, and Shire Pharmaceuticals. Dr. McCracken consults and receives research support from Bristol Myers Squibb, Aspect, Eli Lilly & Company, Wyeth, Sanofi-Aventis, and Pfizer. Drs. Loo, Hale, Shrestha, Nelson, and Smalley, and Mr. Hanada and Mr. Macion report no biomedical financial interests or potential conflicts of interest.

PII: S0890-8567(10)00076-6

doi:10.1016/j.jaac.2010.01.002


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