Abstract:
BACKGROUND:Emerging evidence suggests disruptions in the wiring organization of the brain's network in schizophrenia (SZ) and bipolar disorder (BD). As the importance of genetic predisposition has been firmly established in these illnesses, children (offspring) of patients constitute an at-risk population. This study examines connectome organization in children at familial high risk for psychosis. METHODS:Diffusion-weighted magnetic resonance imaging scans were collected from 127 nonpsychotic offspring 8 to 18 years of age (average age = 13.5 years) of a parent diagnosed with SZ (SZ offspring; n = 28) or BD (BD offspring; N = 60) and community control subjects (n = 39). Resting-state functional magnetic resonance imaging scans were available for 82 subjects. Anatomical and functional brain networks were reconstructed and examined using graph theoretical analysis. RESULTS:SZ offspring were found to show connectivity deficits of the brain's central rich club (RC) system relative to both control subjects and BD offspring. The disruption in anatomical RC connectivity in SZ offspring was associated with increased modularity of the functional connectome. In addition, increased coupling between structural and functional connectivity of long-distance connections was observed in both SZ offspring and BD offspring. CONCLUSIONS:This study shows lower levels of anatomical RC connectivity in nonpsychotic young offspring of SZ patients. This finding suggests that the brain's anatomical RC system is affected in at-risk youths, reflecting a connectome signature of familial risk for psychotic illness. Moreover, finding no RC deficits in offspring of BD patients suggest a differential effect of genetic predisposition for SZ versus BD on the developmental formation of the connectome.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
Collin G,Scholtens LH,Kahn RS,Hillegers MHJ,van den Heuvel MPdoi
10.1016/j.biopsych.2017.06.013subject
Has Abstractpub_date
2017-11-15 00:00:00pages
746-755issue
10eissn
0006-3223issn
1873-2402pii
S0006-3223(17)31712-2journal_volume
82pub_type
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