Genetic Expression Defects Associated with Neurobehavioral Disorders in Rats – conclusion

Delineating the genetic links between genes and behavior may help delineate the etiology of some neurobehavioral disorders such as dyslexia. This paper reviews such a genetic link to dyslexia with subsequent examination of associated behavior in experimental models.

From the review, neurobehavioral disorders observed in animal models may be associated with impaired neuronal migration. Such impairment in migration results from curtailed expressions of genes such as DYX1C, KIAA0319 and DCDC2, which have been identified as candidate genes for dyslexia. This is specifically buttressed by observations that replenishing such expression capabilities, leads to recovery of neuronal migration to almost equal that of cells that had not been targeted for the knockdown of candidate genes. Association of these genes may however not be absolute, since some of the suggested putative alleles have not replicated such association in other populations.

However, whenever genetic mutations result into impaired migration, malformations that correlate with those found in postmortem assays of dyslexics’ brains result. Such malformations include ectopias and mycrogyria in the cortex that are associated with behavioral deficits in auditory processing and working memory in rats treated for suppression of genes associated with susceptibility with dyslexia. Other malformations such as laminar disruptions are associated with curtailed working memory capabilities. Observations that young mice may be more affected as reflected in auditory processing tests than adult mice, also correlate with observations that impairment of neuronal migration following the knockdown of candidate genes is more pronounced in embryonic relative to adult forms. Therefore, genetic mutations could explain some of the neurobehavioral disorders noted in experimental models and, subsequently, such links better the understanding of neurobehavioral disorders affecting individuals.

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