Progress towards a cellular neurobiology of reading disability

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

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cell Movement / genetics
  • Cerebral Cortex / physiopathology*
  • Cytoskeletal Proteins
  • Dyslexia / genetics*
  • Dyslexia / physiopathology*
  • Genetic Predisposition to Disease
  • Humans
  • Microtubule-Associated Proteins / genetics
  • Nerve Tissue Proteins / genetics
  • Neurons / physiology*
  • Nuclear Proteins / genetics

Substances

  • Cytoskeletal Proteins
  • DCDC2 protein, human
  • DNAAF4 protein, human
  • KIAA0319 protein, human
  • Microtubule-Associated Proteins
  • Nerve Tissue Proteins
  • Nuclear Proteins