4.7 Review

Progress towards a cellular neurobiology of reading disability

期刊

NEUROBIOLOGY OF DISEASE
卷 38, 期 2, 页码 173-180

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.06.019

关键词

Dyslexia; Neocortex; Neuronal migration; Development; DCDC2; KIAA0319; DYX1C1

资金

  1. Yale-Rosenberg Genetics Fellowship
  2. NIH [R01 NS43530, R01HD]
  3. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD057853, R01HD055655] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH056524] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS043530] Funding Source: NIH RePORTER

向作者/读者索取更多资源

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.

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