Progress towards a cellular neurobiology of reading disability.
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.
Gabel
Lisa A
LA
Department of Psychology, Lafayette College, Easton, PA, USA.
Gibson
Christopher J
CJ
Gruen
Jeffrey R
JR
LoTurco
Joseph J
JJ
D002465:Cell Movement / Q000235:genetics; D002540:Cerebral Cortex / Q000503:physiopathology*; D003598:Cytoskeletal Proteins; D004410:Dyslexia / Q000235:genetics* / Q000503:physiopathology*; D020022:Genetic Predisposition to Disease; D006801:Humans; D008869:Microtubule-Associated Proteins / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics; D009474:Neurons / Q000502:physiology*; D009687:Nuclear Proteins / Q000235:genetics
D003598:Cytoskeletal Proteins; C510451:DCDC2 protein, human; C478878:DNAAF4 protein, human; C500377:KIAA0319 protein, human; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins