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阅读障碍的细胞神经生物学研究进展。

Progress towards a cellular neurobiology of reading disability.

机构信息

Department of Psychology, Lafayette College, Easton, PA, USA.

出版信息

Neurobiol Dis. 2010 May;38(2):173-80. doi: 10.1016/j.nbd.2009.06.019. Epub 2009 Jul 17.

DOI:10.1016/j.nbd.2009.06.019
PMID:19616627
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2854314/
Abstract

Reading Disability (RD) is a significant impairment in reading accuracy, speed and/or comprehension despite adequate intelligence and educational opportunity. RD affects 5-12% of readers, has a well-established genetic risk, and is of unknown neurobiological cause or causes. In this review we discuss recent findings that revealed neuroanatomic anomalies in RD, studies that identified 3 candidate genes (KIAA0319, DYX1C1, and DCDC2), and compelling evidence that potentially link the function of candidate genes to the neuroanatomic anomalies. A hypothesis has emerged in which impaired neuronal migration is a cellular neurobiological antecedent to RD. We critically evaluate the evidence for this hypothesis, highlight missing evidence, and outline future research efforts that will be required to develop a more complete cellular neurobiology of RD.

摘要

阅读障碍(RD)是一种尽管智力和教育机会充足,但在阅读准确性、速度和/或理解方面存在显著障碍的疾病。RD 影响 5-12%的读者,具有明确的遗传风险,且其神经生物学原因或原因尚不清楚。在这篇综述中,我们讨论了最近的发现,这些发现揭示了 RD 中的神经解剖异常、确定了 3 个候选基因(KIAA0319、DYX1C1 和 DCDC2)的研究,以及强有力的证据表明候选基因的功能与神经解剖异常之间存在潜在联系。一个假说已经出现,即神经元迁移受损是 RD 的细胞神经生物学前体。我们批判性地评估了这一假说的证据,强调了缺失的证据,并概述了未来需要开展的研究工作,以进一步发展 RD 的更完整的细胞神经生物学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6076/2854314/ae85f0215c6f/nihms133459f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6076/2854314/ae85f0215c6f/nihms133459f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6076/2854314/ae85f0215c6f/nihms133459f1.jpg

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Knockout Mice for Dyslexia Susceptibility Gene Homologs KIAA0319 and KIAA0319L have Unaffected Neuronal Migration but Display Abnormal Auditory Processing.阅读障碍易感基因同源物 KIAA0319 和 KIAA0319L 的敲除小鼠神经元迁移正常,但听觉处理异常。
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