Genetic Expression Defects Associated with Neurobehavioral Disorders in Rats

The identification of clear links between genes and behavior may help delineate the etiology of some neurobehavioral disorders. One such disorder whose occurrence is noted to arise with gene variants or mutations is dyslexia. Although dyslexia and reading disability (RD) are at times considered different due to the “additional spelling and writing impairments associated with … RD” (Gabel et al. 174), most studies have considered these disorders to be synonymous (e.g. Paracchini et al. 1659; Meng et al. 17053) – a perspective that this paper adopts. By definition, developmental dyslexia is a learning disability that manifests as a significantly impaired learning in the affected individuals, despite such individuals having normal intelligence, appropriate motivation and availed with the relevant educational opportunity (Rosen et al. 2562; Gabel et al. 173; Paracchini et al. 1659; Meng et al. 17053). In terms of prevalence, RD has been noted to affect 5-12% of school-age children (Gabel et al. 174), but some studies have put the prevalence rates to extend to 17% (Shaywitz qtd. in Meng et al. 17053).

Despite the neurological and cognitive basis of dyslexia remaining ambiguous (Paracchini et al. 1659), various observations link dyslexia to a genetic antecedent. Firstly, RD cases are “highly familial and heritable” (Paracchini et al. 1659). Secondly, RD is associated with impaired migration of neurons in neocortex (Wang et al. 515), which studies have attributed to curtailed expression of specific genes (Paracchini et al. 1659).  One of the candidate genes, which was first to be linked with vulnerability for dyslexia, is DYX1C1 (Wang et al. 515). Other studies have subsequently noted susceptibility in KIAA0319 and DCDC2 genes and, to a lesser extent, ROBO1 is also a suggested candidate (Galaburda et al. 1213; Meng et al. 17053; Paracchini et al. 1659). Observations of abnormalities in neocortical neuronal migration such as “molecular layer heteropias, laminar dysplasias, and periventricular nodular erotopias” in brains of dyslexics, in post-mortem assays have reinforced such association (Rosen et al. 2562). Further, animal studies have provided a causal relationship between such impaired cortical migration of neurons and curtailed perception and learning (Gabel, et al. 174). Accordingly, attempts to delineate the pathways that link genes to behavior, provides a basis to enhanced understanding of neurobehavioral disorders that are associated with a genetic etiology (Galaburda et al. 1213).

This paper follows such a quest, its purpose being to highlight the link between genetic expression defects and neurobehavioral disorders, especially dyslexia, in rats. Specifically, the paper will highlight how normal expression of the respective genes affects brains function, and what alterations that impaired expression causes in the brain, that lead to neurobehavioral disorders such as dyslexia. The discussions in the paper are ordered into different sections; the introduction provides a brief overview of genetic link to neurobehavioral disorders such as dyslexia. The subsequent section comprises a literature review, organized into a part discussing the link between genes and dyslexia, a part discussing the various aspects of the implicated genes such as functions in normal and abnormal statuses, and, the third aspect of the literature review, considers the animal models used to assess the genetic link to dyslexia and how such genetic malformations are associated with specific behavior in such animals. Finally, the paper provides a conclusion that links the core points highlighted throughout. Go to part 2 here.

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