Network asymmetry, callosal development and autistic behaviour

本研究旨在整合人类成像和小鼠模型的信息，以验证胼胝体（CC）缺陷可以影响联合白色物质（WM）的发展，以及自闭症谱系障碍（ASD）中发生的缺陷的假设。它旨在测试：在小鼠模型中，（1）如果CC的非典型发展破坏了相关WM途径的发展（2）如果CC缺陷与ASD样表型相关（使用ASD候选基因突变的小鼠）在灵长类动物中的应用，包括患有ASD的发育中的人类和成年人（3）如果猕猴/长尾猴之间存在物种特异性CC差异，黑猩猩和人类（4）如果CC微结构解剖与语言和社会认知相关的关联途径的正常不对称发展有关（5）如果CC缺陷与关联WM途径中的缺陷有关（6）如果这些缺陷与症状相关

This study aims to integrate information from human imaging and mouse models to test the hypothesis that deficits in the corpus callosum (CC) can impact the development of association white matter (WM), and that such deficits occur in Autism Spectrum Disorder (ASD). It aims to test: in mouse-models(1) if non-typical development of the CC disrupts development of association WM pathways(2) if CC deficits correlate with ASD-like phenotypes (using mice with mutations in ASD candidate genes) in primates, including developing humans and adults with ASD(3) if species-specific CC differences exist between Macaque/Vervet monkeys, Chimpanzees and Humans(4) if CC microstructural anatomy is linked to normal asymmetry development of association pathways involved inlanguage and social cognition(5) if deficits of the CC correlate with those in association WM pathways(6) if such deficits correlate with symptoms