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- W1799457674 abstract "Genetically Williams syndrome (WS) promises to provide essential insight into the pathophysiology of cortical development because its ∼28 deleted genes are crucial for cortical neuronal migration and maturation. Phenotypically, WS is one of the most puzzling childhood neurodevelopmental disorders affecting most intellectual deficiencies (i.e. low-moderate intelligence quotient, visuospatial deficits) yet relatively preserving what is uniquely human (i.e. language and social-emotional cognition). Therefore, WS provides a privileged setting for investigating the relationship between genes, brain and the consequent complex human behaviour.We used in vivo anatomical magnetic resonance imaging analysing cortical surface-based morphometry, (i.e. surface area, cortical volume, cortical thickness, gyrification index) and cortical complexity, which is of particular relevance to the WS genotype-phenotype relationship in 22 children (2.27-14.6 years) to compare whole hemisphere and lobar surface-based morphometry between WS (n = 10) and gender/age matched normal controls healthy controls (n = 12).Compared to healthy controls, WS children had a (1) relatively preserved Cth; (2) significantly reduced SA and CV; (3) significantly increased GI mostly in the parietal lobe; and (4) decreased CC specifically in the frontal and parietal lobes.Our findings are then discussed with reference to the Rakic radial-unit hypothesis of cortical development, arguing that WS gene deletions may spare Cth yet affecting the number of founder cells/columns/radial units, hence decreasing the SA and CV. In essence, cortical brain structure in WS may be shaped by gene-dosage abnormalities." @default.
- W1799457674 created "2016-06-24" @default.
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- W1799457674 date "2011-11-02" @default.
- W1799457674 modified "2023-10-10" @default.
- W1799457674 title "Williams syndrome: a relationship between genetics, brain morphology and behaviour" @default.
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- W1799457674 doi "https://doi.org/10.1111/j.1365-2788.2011.01490.x" @default.
- W1799457674 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22044458" @default.
- W1799457674 hasPublicationYear "2011" @default.
- W1799457674 type Work @default.