Abstract
Williams syndrome (WS) and 7q11.23 duplication syndrome (Dup7) are caused by hemideletion or duplication, respectively, of ∼25 genes on chromosomal locus 7q11.23. Previous research has shown altered functional connectivity and white-matter microstructure in WS. After searching across the brain for regions with altered functional connectivity related to 7q11.23 copy number variation (CNV), we tested for alterations in white-matter tracts connecting these regions as a function of gene dosage.
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