Linkage analysis has revealed a number of gene intervals conferring susceptibility to developmental dyslexia (DD)—a language-based learning disability affecting 4–10% of the population. While the specific causes of dyslexia are not yet known, the isolation of the DD functional genes has ushered the new era of understanding the link between genetics and cognitive functions. With our recent accumulating data, a connection between disruptions in neuronal architecture and genetic susceptibility to development dyslexia (DD) is highly suggested. Here, we explored the functions of two dyslexia susceptibility genes, DYX1C1 and DCDC2, in rodent cerebral cortex. The results from our study indicate that DYX1C1 plays a role in the migration of neocortical neurons and more specifically is required for the transition out of the multipolar stage of migration. We also demonstrated that Dcdc2 is a microtubule associated protein and functions not only in neuronal migration but also neuritic growth. Additionally, our data displayed that DCDC2 and DCX are partially functionally redundant in neurodevelopment. These genetic and neurobiological evidence has strengthened a working hypothesis that dyslexia is caused by early developmental disruptions that subsequently cause functional impairments in neocortical circuits.
|Advisor:||LoTurco, Joseph J.|
|School:||University of Connecticut|
|School Location:||United States -- Connecticut|
|Source:||DAI-B 72/10, Dissertation Abstracts International|
|Keywords:||Dyslexia, Neurodevelopment, Neuron migration|
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