The corpus callosum is implicated in the pathophysiology of autism spectrum disorder (ASD). However, specific structural deficits and underlying mechanisms are yet to be well defined. We employed diffusional kurtosis imaging (DKI) metrics to characterize white matter properties within five discrete segments of the corpus callosum in 17 typically developing (TD) adults and 16 age-matched participants with ASD without co-occurring intellectual disability (ID). The DKI metrics included axonal water fraction (faxon) and intra-axonal diffusivity (Daxon), which reflect axonal density and caliber, and extra-axonal radial (RDextra) and axial (ADextra) diffusivities, which reflect myelination and microstructural organization of the extracellular space. The relationships between DKI metrics and processing speed, a cognitive feature known to be impaired in ASD, were also examined. ASD group had significantly decreased callosal faxon and Daxon (p = .01 and p = .045), particularly in the midbody, isthmus, and splenium. Regression analysis showed that variation in DKI metrics, primarily in the mid and posterior callosal regions explained up to 70.7% of the variance in processing speed scores for TD (p = .001) but not for ASD (p > .05). Decreased DKI metrics suggested that ASD may be associated with axonal deficits such as reduced axonal caliber and density in the corpus callosum, especially in the mid and posterior callosal areas. These data suggest that impaired interhemispheric connectivity may contribute to decreased processing speed in ASD participants.

中文翻译：

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自闭症call体的扩散峰度成像

call体与自闭症谱系障碍（ASD）的病理生理有关。但是，具体的结构缺陷和潜在机制尚待明确。我们采用扩散峰度成像（DKI）指标来表征17名典型发育中（TD）成人和16名年龄相匹配的ASD参与者的without体五个离散节段内的白质特性，而没有同发性智障（ID）。DKI指标包括反映轴突密度和口径的轴突水分数（faxon）和轴突内扩散率（Daxon），以及轴突外径向（RDextra）和轴突（ADextra）扩散率，它们反映了细胞外髓鞘化和微结构的组织空间。DKI指标与处理速度之间的关系，还检查了已知在ASD中受损的认知功能。ASD组的call骨fax和Daxon明显减少（p = 0.01和p = 0.045），特别是在中体，峡部和脾脏中。回归分析表明，DKI指标的变化（主要在call骨中部和后部区域）解释了TD处理速度得分差异的70.7％（p = .001），而不是ASD（p> .05）。DKI指标降低提示ASD可能与轴突缺陷有关，例如call体特别是中部和后部areas体的轴突口径和密度降低。这些数据表明，半球间连通性受损可能会导致ASD参与者的处理速度降低。01和p = .045），特别是在中体，峡部和脾中。回归分析表明，DKI指标的变化（主要在call骨中部和后部区域）解释了TD处理速度得分差异的70.7％（p = .001），而不是ASD（p> .05）。DKI指标降低提示ASD可能与轴突缺陷有关，例如call体特别是中部和后部areas体的轴突口径和密度降低。这些数据表明，半球间连通性受损可能会导致ASD参与者的处理速度降低。01和p = .045），特别是在中体，峡部和脾中。回归分析表明，DKI指标的变化（主要在call骨中部和后部区域）解释了TD处理速度得分差异的70.7％（p = .001），而不是ASD（p> .05）。DKI指标降低提示ASD可能与轴突缺陷有关，例如call体特别是中部和后部areas体的轴突口径和密度降低。这些数据表明，半球间连通性受损可能会导致ASD参与者的处理速度降低。TD（p = .001）的处理速度得分方差的7％（ASD（p> .05）则不是）。DKI指标降低提示ASD可能与轴突缺乏有关，例如call体，特别是中部和后部areas体的轴突口径和密度降低。这些数据表明，半球间连通性受损可能会导致ASD参与者的处理速度降低。TD（p = .001）的处理速度得分方差的7％（ASD（p> .05）则不是）。DKI指标降低提示ASD可能与轴突缺乏有关，例如call体，特别是中部和后部areas体的轴突口径和密度降低。这些数据表明，半球间连通性受损可能会导致ASD参与者的处理速度降低。