Skip to main content
 

Neural correlates of abstract social cognition in Williams syndrome and 7q11.23 Duplication syndrome

Thursday, September 14, 2017 — Poster Session III

12:00 p.m. – 1:30 p.m.
FAES Terrace
NIMH
NEURO-24

Authors

  • DL Currin
  • TA Nash
  • M Jabbi
  • DP Eisenberg
  • MD Gregory
  • KV Roe
  • R Prabhakaran
  • J Carrasco
  • O Ravindranath
  • SE Grogans
  • MM O'Brien
  • JS Kippenhan
  • P Kohn
  • A Martin
  • CB Mervis
  • KF Berman

Abstract

Hemideletion (yielding one copy of affected genes) or duplication (three gene copies) of ~25 genes at chromosomal location 7q11.23 causes Williams syndrome (WS) or 7q11.23 Duplication syndrome (DUP7), respectively. While children with WS show hypersociability and increased empathy, children with DUP7 have reduced sociability and heightened systemizing. In this study, we used fMRI to study abstract social cognition in children with WS and DUP7, as well as typically developing (TD) children. During 3T fMRI, 13 children with WS (age=13.5±3.6, 10 girls), 31 TD children (age=13.9±3.6, 13 girls), and 11 children with DUP7 (age=12.9±3.1, 5 girls) watched videos of moving geometric shapes that could be interpreted as social interactions, and, as a control task, videos of the same shapes moving randomly. After preprocessing with SPM5, we ran ANOVAs to test for group differences in BOLD activation (social vs. control task, p

Category: Neuroscience