PT  - JOURNAL ARTICLE
AU  - Wenhao Jiang
AU  - Kuaikuai Duan
AU  - Kelly Rootes-Murdy
AU  - Pieter J. Hoekstra
AU  - Catharina Hartman
AU  - Jaap Oosterlaan
AU  - Dirk Heslenfeld
AU  - Barbara Franke
AU  - Jan Buitelaar
AU  - Alejandro Arias-Vasquez
AU  - Jingyu Liu
AU  - Jessica A. Turner
TI  - Structural Brain Alterations and Their Association with Cognitive Function and Symptoms in Attention-Deficit/Hyperactivity Disorder Families
AID  - 10.1101/863605
DP  - 2019 Jan 01
TA  - bioRxiv
PG  - 863605
4099  - http://biorxiv.org/content/early/2019/12/04/863605.short
4100  - http://biorxiv.org/content/early/2019/12/04/863605.full
AB  - Gray matter disruptions have been found consistently in Attention-deficit/Hyperactivity Disorder (ADHD). The organization of these alterations into brain structural networks remains largely unexplored. We investigated 508 participants (281 males) with ADHD (N = 210), their unaffected siblings (N = 108), individuals with subthreshold ADHD (N = 49), and unrelated healthy controls (N = 141) with an age range from 7 – 18 years old from 336 families in the Dutch NeuroIMAGE project. Source based morphometry was used to examine structural brain network alterations and their association with symptoms and cognitive performance. Two networks showed significant reductions in individuals with ADHD compared to unrelated healthy controls after False Discovery Rate correction. Component A, mainly located in bilateral Crus I, showed a case/control difference with sub-clinical cases being intermediate between cases and controls. The unaffected siblings were similar to controls. After correcting for IQ and medication status, component A showed a negative correlation with inattention symptoms across the entire sample. Component B included a maximum cluster in the bilateral insula, where unaffected siblings, similar to cases, showed significantly reduced loadings compared to controls; but no relationship with individual symptoms or cognitive measures was found for component B. This multivariate approach suggests that areas reflecting genetic liability within ADHD are partly separate from those areas modulating symptom severity.