期刊
NEUROIMAGE-CLINICAL
卷 27, 期 -, 页码 -出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.nicl.2020.102273
关键词
ADHD; Independent component analysis; Cerebellum; Insula; Inattention
类别
资金
- National Institutes of Health
- National Institute of Mental Health [1R01MH106655]
- NIH [R01MH62873]
- NWO Large Investment Grant [1750102007010]
- Radboud University Medical Center, University Medical Center Groningen and Accare
- VU University Amsterdam
- NWO Brain Cognition [43309-242, 056-13-015]
- ZonMW [60-60600-97-193]
- European Union's FP7 program [278948, 602450, 602805]
- European Union [667302, 728018]
- Netherlands Organization for Scientific Research (NWO) [433-09-229, 016-130-669]
- Dutch National Research Agenda for the NeuroLabNL project
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 to 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 ADHD/typically developing difference with subthreshold cases being intermediate between ADHD and typically developing 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 individuals with ADHD, 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.
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