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The molecular genetics and neurobiology of developmental dyslexia as model of a complex phenotype

机译:发育综合症的分子遗传学和神经生物学作为复合表型模型的模型

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摘要

Among complex disorders, those concerning neuropsychiatric phenotypes involve particular challenges compared to disorders with more easily distinguished clinical signs and measures. One such common and unusually challenging phenotype to disentangle genetically is developmental dyslexia (DD), or reading disability, defined as the inability to learn to read and write for an otherwise normally intelligent child with normal senses and educational opportunity. There is presently ample evidence for the strongly biological etiology for DD, and a dozen susceptibility genes have been suggested. Many of these genes point to common but previously unsuspected biological mechanisms, such as neuronal migration and cilia functions. I discuss here the state-of-the-art in genomic and neurobiological aspects of DD research, starting with short general background to its history. (C) 2014 The Author. Published by Elsevier Inc.
机译:在复杂的障碍中,与具有更容易尊重的临床症状和措施的疾病相比,那些有关神经精神表型的那些涉及特殊挑战。 一种如此常见的和异常挑战的表型遗传遗传是发育综合症(DD)或阅读残疾,定义为无法学习读写具有正常感官和教育机会的通常聪明的孩子。 目前有充分的证据表明DD的强烈生物学病因,并提出了十几种易感性基因。 这些基因中的许多基因指向常见但以前未经用过的生物机制,例如神经元迁移和纤毛功能。 我在这里讨论了DD研究的基因组和神经生物学方面的最先进,从近一般的背景开始到其历史。 (c)2014提交人。 elsevier公司发布

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