As originally planned, the ROO phase research will continue at UCLA. Hence, plans for the ROO phase, including research protocol and personnel, remain as originally proposed barring one instance. Dr. Andrew Leuchter will not serve as an EEG consultant as originally proposed. This change reflects new resources integrated to our group that provide abundant access to EEG expertise (example: through Dr. Sandra Loo and her colleagues, as well as my developed expertise over the last two years). Through the K99 phase I have greately increased my skill in neurogenetic research methodology. Moreover, in conjunction with our research group I have completed behavioral and EEG assessment of hemispherically specialized information processing (lateralized information processing-LIP) on 300 families with two affected ADHD siblings, and identified several LIP endophenotypes by evidence of familiality and association with neurocognitive variants underlying behavioral constructs in ADHD. Furthermore, this vyork has uncovered highly significant LIP-gene associations that have inspired a key co-investigator (Dr. Geschwind) to volunteer resources for genotyping of laterality candidate genes in our sample. Indeed, K99 phase of this award has e well position to begin the independent research phase further investigating the association between genes and their expression on LIP in children with ADHD. As originally proposed, this work will investigate the genetics of LIP and its association with ADHD via data 6dllection of a control sample matched to the previously collected ADHD sample of children and adolescents in order to 1) analyze the strength of association of lateralized brain function (behavioral, EEG, fMRI) with ADHD status, 2) analyze the relationship of cognitive deficits with LIP in ADHD and control samples; and 3) identify genes involved in the neurogenesis of LIP using identified endophenotypes (through case/control analysis) and traditional gene detection methods (quantitative trariSfnission disequilibiium:|ssting-QTDT) and gene expression arrays in our larger sample of 300 families with two ADHD, affected offspring.