Date of Award

Fall 12-20-2019

Degree Type

Dissertation

Degree Name

Ph.D.

Degree Program

Applied Biopsychology

Department

Psychology

Major Professor

Beaton, Elliott

Second Advisor

Knaus, Tracey

Third Advisor

Scalco, Matthew

Fourth Advisor

Black, Sarah

Abstract

Neurological abnormalities are associated with emotion processing deficits seen in children with neurodevelopmental disorders. Research suggests that inflammatory mechanisms can negatively impact brain structure and function and are thought to play a role in these processing atypicalities. Children with chromosome 22q11.2 deletion syndrome (22q11.2DS) exhibit emotion processing impairments and associated neural abnormalities. We investigated the roles of inflammatory factors and structural connectivity in relation to emotion processing deficits in 28 children with 22q11.2DS and 33 typically developing children (M = 11.12 years old; SD = 2.17). Results indicate poorer social skills and significantly lower emotion recognition scores in children with 22q11.2DS compared to controls. Additionally, children with 22q11.2DS had higher anisotropic diffusion in right amygdala to fusiform gyrus white matter pathways and lower serum IL-3 concentrations than their typically developing peers. Right amygdala to fusiform gyrus FA values partially mediated the relationship between 22q11.2DS and social skills, as well as the relationship between 22q11.2DS and emotion recognition accuracy. However, there was no indication that IL-3 mediated the relationship between diagnosis and abnormal connectivity. Future studies should employ longitudinal methods to characterize how these connectivity patterns influence social-emotional development as the child ages.

Rights

The University of New Orleans and its agents retain the non-exclusive license to archive and make accessible this dissertation or thesis in whole or in part in all forms of media, now or hereafter known. The author retains all other ownership rights to the copyright of the thesis or dissertation.

Available for download on Friday, December 20, 2024

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