Progress towards a cellular neurobiology of reading disability

被引：41

作者：

Gabel, Lisa A. ^{[2
,3
]}

Gibson, Christopher J. ^{[4
]}

Gruen, Jeffrey R. ^{[4
,5
,6
]}

LoTurco, Joseph J. ^{[1
]}

机构：

[1] Univ Connecticut, Dept Physiol & Neurobiol, Storrs, CT 06268 USA

[2] Lafayette Coll, Dept Psychol, Easton, PA 18042 USA

[3] Lafayette Coll, Program Neurosci, Easton, PA 18042 USA

[4] Yale Univ, Sch Med, Dept Pediat, Yale Child Hlth Res Ctr, New Haven, CT 06510 USA

[5] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA

[6] Yale Univ, Sch Med, Program Med, Dept Invest, New Haven, CT USA

来源：

NEUROBIOLOGY OF DISEASE | 2010年 / 38卷 / 02期

关键词：

Dyslexia; Neocortex; Neuronal migration; Development; DCDC2; KIAA0319; DYX1C1; PERIVENTRICULAR NODULAR HETEROTOPIA; NEURONAL MIGRATION DISORDER; QUANTITATIVE-TRAIT LOCUS; DOUBLECORTIN-LIKE-KINASE; DEVELOPMENTAL DYSLEXIA; NEOCORTICAL ECTOPIAS; GENETIC INFLUENCES; WHITE-MATTER; SUSCEPTIBILITY GENE; BXSB MICE;

D O I：

10.1016/j.nbd.2009.06.019

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：173 / 180

页数：8

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