Progress towards a cellular neurobiology of reading disability

NEUROBIOLOGY OF DISEASE

卷:38

Review

Gabel, Lisa A.^2,3  Gibson, Christopher J.⁴  Gruen, Jeffrey R.^4,5,6  LoTurco, Joseph J.¹ 

[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

关键词: Dyslexia;    Neocortex;    Neuronal migration;    Development;    DCDC2;    KIAA0319;    DYX1C1;   

DOI  :  10.1016/j.nbd.2009.06.019

来源: Elsevier

【 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.

【 授权许可】

Free