一项研究报告说，大脑皮层是覆盖着大脑的一层灰色物质，它们能影响有意识的思维、记忆、语言和其他功能，在大脑皮层内部神经连线的差别可能预测有自闭症谱系障碍（ASD）的成年人的社会与重复症状的严重程度。成像研究已经提示，在患自闭症和没有患自闭症的人的白质内部信号以不同的方式通信，但是仍然不清楚皮层的灰质内部的神经连线如何受到影响。ChristineEcker及其同事探索了患自闭症谱系障碍（ASD）的人们与一般人群的正确连接这个皮层内部区域所需的连接长度的差异。这组作者对患有自闭症谱系障碍（ASD）和没有患有该病的68名成年人进行了磁共振成像（MRI）扫描，结果发现患自闭症的人的连线成本远远低于没有患自闭症的人，特别是在大脑的前颞叶区域。这组作者说，这些发现证实了患自闭症谱系障碍（ASD）的人们的大脑的白质和灰质中都存在不寻常的连接，而且发现了可能是自闭症症状的基础的一组核心的神经变化。（生物谷Bioon.com）
生物谷推荐的英文摘要
PNAS doi: 10.1073/pnas.1221880110
Intrinsic gray-matter connectivity of the brain in adults with autism spectrum disorder
Christine Eckera,1,2, Lisa Ronanb,1, Yue Fenga, Eileen Dalya, Clodagh Murphya, Cedric E. Ginestetc, Michael Brammerc, Paul C. Fletcherb, Edward T. Bullmoreb, John Sucklingb, Simon Baron-Cohend, Steve Williamsc, Eva Lotha, MRC AIMS Consortium3, and Declan G. M. Murphy
Autism spectrum disorders (ASD) are a group of neurodevelopmental conditions that are accompanied by atypical brain connectivity. So far, in vivo evidence for atypical structural brain connectivity in ASD has mainly been based on neuroimaging studies of cortical white matter. However, genetic studies suggest that abnormal connectivity in ASD may also affect neural connections within the cortical gray matter. Such intrinsic gray-matter connections are inherently more difficult to describe in vivo but may be inferred from a variety of surface-based geometric features that can be measured using magnetic resonance imaging. Here, we present a neuroimaging study that examines the intrinsic cortico-cortical connectivity of the brain in ASD using measures of “cortical separation distances” to assess the global and local intrinsic “wiring costs” of the cortex (i.e., estimated length of horizontal connections required to wire the cortex within the cortical sheet). In a sample of 68 adults with ASD and matched controls, we observed significantly reduced intrinsic wiring costs of cortex in ASD, both globally and locally. Differences in global and local wiring cost were predominantly observed in fronto-temporal regions and also significantly predicted the severity of social and repetitive symptoms (respectively). Our study confirms that atypical cortico-cortical “connectivity” in ASD is not restricted to the development of white-matter connections but may also affect the intrinsic gray-matter architecture (and connectivity) within the cortical sheet. Thus, the atypical connectivity of the brain in ASD is complex, affecting both gray and white matter, and forms part of the core neural substrates underlying autistic symptoms.
