The DCDC2 Intron 2 Deletion Impairs Illusory Motion Perception Unveiling the Selective Role of Magnocellular-Dorsal Stream in Reading (Dis)ability
The DCDC2 Intron 2 Deletion Impairs Illusory Motion Perception Unveiling the Selective Role of Magnocellular-Dorsal Stream in Reading (Dis)ability
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DOI：
10.1093/cercor/bhu234
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发表时间：
2015-06-01
期刊：
影响因子：
3.7
通讯作者：
Marino, Cecilia
中科院分区：
文献类型：
--
作者：
Gori, Simone;Mascheretti, Sara;Marino, Cecilia
发展性阅读障碍（DD）是一种遗传性神经发育性阅读障碍，可由听觉、视觉和跨通道整合缺陷引起。DCDC 2基因内含子2的缺失（以下简称DCDC 2d）增加了DD和相关表型的风险。在这项研究中，首先，我们报告说，虚幻的视觉运动知觉，特别是处理的magnocellular-dorsal（MD）流，是受损的DD儿童相比，年龄匹配和阅读水平的控制。其次，我们测试了DCDC 2d对M-D流的影响的特异性。与DD和DCDC 2d的儿童需要显着更多的对比度，以处理虚幻的运动相对于他们的同行没有DCDC 2d和年龄匹配和阅读水平的控制。不管遗传变异，DD儿童在小细胞腹侧任务中表现正常。最后，我们发现，DCDC 2d也与成人正常读者的错觉运动知觉，表明M-D缺陷是一个潜在的神经生物学危险因素的DD，而不是一个简单的影响阅读障碍。我们的研究结果首次表明，一种特定的神经认知功能障碍与明确的遗传易感性有关。
Developmental dyslexia (DD) is a heritable neurodevelopmental reading disorder that could arise from auditory, visual, and cross-modal integration deficits. A deletion in intron 2 of the DCDC2 gene (hereafter DCDC2d) increases the risk for DD and related phenotypes. In this study, first we report that illusory visual motion perception-specifically processed by the magnocellular-dorsal (M-D) stream-is impaired in children with DD compared with age-matched and reading-level controls. Second, we test for the specificity of the DCDC2d effects on the M-D stream. Children with DD and DCDC2d need significantly more contrast to process illusory motion relative to their counterpart without DCDC2d and to age-matched and reading-level controls. Irrespective of the genetic variant, children with DD perform normally in the parvocellular-ventral task. Finally, we find that DCDC2d is associated with the illusory motion perception also in adult normal readers, showing that the M-D deficit is a potential neurobiological risk factor of DD rather than a simple effect of reading disorder. Our findings demonstrate, for the first time, that a specific neurocognitive dysfunction tapping the M-D stream is linked with a well-defined genetic susceptibility.