In sum, our results demonstrate that the reading problems experienced by children with dyslexia are not a consequence of visual magnocellular dysfunction. While visual magnocellular weakness does manifest in dyslexia, it is not the cause of the reading problem. Second, the weaknesses in the magnocellular visual system, indexed in this

study by the amount of activity in area V5/MT during the perception of visual motion, do not represent a symptom of dyslexia. They are not, Tariquidar manufacturer as previous models assumed, part of a common etiology with different behavioral manifestations and thereby an integral part of the pathophysiology of dyslexia. Rather, they are a secondary consequence of reading experience itself. We suggest that phonological deficits, by restricting the amount and quality of reading in dyslexics, limit the opportunity for reading to induce changes in the visual magnocellular system (by mechanisms that remain to be determined). As such, reading itself can be thought of as an environmental influence that bears on functional and anatomical aspects of the brain and, in the case of reading disability, these changes are not invoked to the same degree as they are in typical Bortezomib concentration readers. In the context of the observed differences at the level of the LGN, larger neurons in the controls relative to the dyslexic at postmortem could be due to extensive versus limited experience with reading over

a lifetime. The same explanation holds to account for the differences between dyslexics and age-matched controls in behavioral studies

of magnocellular function and brain imaging studies of V5/MT. Together, our results represent not only an important advancement in understanding the etiology of developmental dyslexia, but also offer a reinterpretation of the existing data on visual magnocellular dysfunction in dyslexia. They also contribute to an important growing body of work that explains how experience, in this case for reading, alters the functional organization of the brain. Subjects participating in all three experiments were native English speakers with no history of neurological or psychiatric disorder, and all Chlormezanone had normal or corrected-to-normal visual acuity. Written informed consent was obtained from the subjects themselves or from the subjects’ parents (in the case of pediatric participants), and all procedures were approved by the Georgetown University Institutional Review Board. All subjects completed a battery of behavioral tests to evaluate intelligence and proficiency on reading and reading-related skills, including the Wechsler Abbreviated Scale of Intelligence Verbal and Performance tests (IQ), Woodcock-Johnson III (WJ-III) Word Identification (WID, single real word reading), and Woodcock-Johnson Word Attack (WA, single pseudoword reading). Subjects in Experiment 3 also completed the Lindamood Auditory Conceptualization Test (LAC-3, phonemic awareness).