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This thesis investigates the nature of atypical attention in relation to autism spectrum disorders (ASD) symptoms, as well as the mechanisms by which it may relate to social impairment. First, does atypical non-social attention predict social impairment over time in the context of ASD, suggestive of a causal relationship? Second, if atypical attention plays a role in social impairments in ASD, what is the mechanism? With regards to the first question, longitudinal data with children at familial risk for ASD demonstrated a unidirectional relationship between non-social attention and social functioning at the cognitive level: 2-year-old non-social attention predicted 3- year-old face recognition, but there was no relationship between 2-year-old face popout and 3-year-old visual search. Additionally, we examined the relationships between ASD and ADHD symptoms over three years in children at high risk for both—children with fragile X syndrome. This allowed for investigating atypical non-social attention and social impairment at the symptoms level, again revealing a unidirectional relationship with ADHD symptoms predicting ASD symptoms over time but not the reverse. These findings suggest that atypical non-social attention may contribute to social impairment. With regards to the second question, a novel eye-tracking and visual search paradigm revealed how task irrelevant social stimuli in natural scenes can lead to poorer subsequent explicit spatial contextual memory and altered memory-guided attention orienting - effects that were moderated by autistic traits and social anxiety within a neurotypical population. Further, this research found cross-sectional development, comparing 6-10-year-old children to young adults, and investigated the neural markers of social stimuli's effect on memory. These studies suggest a possible mechanism whereby a reduced social attention bias could lead autistic individuals to learn and remember less about people and the social world and result in social impairment.

Thesis (Ph.D.) - Simon Fraser University, 2006. / Theses (Dept. of Psychology) / Simon Fraser University. Also issued in digital format and available on the World Wide Web.

Thesis (Ph.D.)--Tufts University, 1999. / Adviser: Holly A. Taylor. Submitted to the Dept. of Psychology. Includes bibliographical references (leaves 59-61). Access restricted to members of the Tufts University community. Also available via the World Wide Web;

Thesis (Ph. D.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains vii, 78 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 34-38).

Thesis (M.S.)--University of Wisconsin--Madison, 1970. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

There is a growing body of evidence linking poor working memory skills, particularly central executive functioning, with lower levels of cognitive attainment throughout the school years. Although the role of the phonological loop in reading development has been well established, there is less agreement as to the role of the central executive. Research suggests that the central executive develops through the early school years as children learn to read, and that this is crucial to the development of fluent word reading. It is also suggested that central executive skills may fail to develop effectively in dyslexic children. The longitudinal study reported here examines the development of working memory and central executive skills in relation to cognitive attainment in the early years of schooling. Children were screened in their Reception year at four/five years old using a dyslexia screening test and a phonological abilities test, and were allocated to one of three groups according to their risk of reading difficulties (At Risk, Middle, Not At Risk). The groups were matched for age. Assessment in school Years 1, 2 and 3 included measures of reading, spelling and mathematics, working memory and central executive functioning. Results indicate that those children showing the greatest number of indicators for dyslexia are falling behind in their cognitive attainment by the age of five to six, and that the At Risk group score significantly lower than the other groups on measures of central executive fbnctioning, especially inhibition. These differences remain significant when non-verbal intelligence, memory capacity and processing speed are controlled for. Further results using standardized working memory tests and experimental data support these conclusions. Examination of teacher ADHD ratings suggests that working memory deficits are identified as attentional problems. The results are discussed in terms of their implications for theory and educational practice.

Early growth response gene – 1 (Egr1) encodes a protein widely present in mammalian body, such as connective tissue, cardiac tissue, the liver, and the brain. As a transcription factor (TF), it is involved in processes that take place in the endocrine, digestive, immune, musculo-skeletal and central nervous systems, for instance, B cell maturation upon B cell receptor activation, tendon repair upon mechano-stimulation, and long-term spatial memory formation. In mammalian brains, EGR1 controls the responses to environmental stimuli such as chronic stress and physical contact. It also participates in processes such as long-term memory consolidation and synapse re-structuring. It plays a role in enacting responses and qualities of gene transcription cascades upon neuronal stimulation. Inside the epigenetic realm, EGR1 recruits Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) to remove DNA methylation at target loci. Due to its critical functions during brain development and upon neuronal activation, mis-regulation of EGR1 is associated with neuropsychological disorders such as post-traumatic stress disorder (PTSD) and schizophrenia (SCZ) in humans. In this study, we performed bioinformatics analysis with brain methylomes and predicted EGR1 may interact with myocyte enhancer factor 2C (MEF2C), which is known to be involved in many similar processes as EGR1, such as synapse architecture, cell migration, and learning and memory. EGR1 and MEF2C ChIP-seq data derived from mouse frontal cortex suggest these two proteins may regulate a common set of downstream genes. To begin, co-immunoprecipitation experiments were performed with HEK293T cells co-transfected with EGR1-FLAG and MEF2C-HA tagged constructs, allowing for specific interaction identification without endogenous protein expression interference. Furthermore, co-immunoprecipitation experiments performed with brain tissues additionally indicated the two proteins interact with each other endogenously. Altogether, this study provides protein-protein interaction evidence for EGR1 and MEF2C in cultured HEK293 cells and in the cortices of adult male mice. This information provides a foundation for future examinations of how these two TFs interact to initiate cascading events following neuronal stimulation. / Master of Science / Early growth response gene – 1 (EGR1) encodes a protein that can be found in animals such as fruit flies, mice, rats, and humans. In mammals, it is widely expressed in the cardiovascular, endocrine, digestive, immune, musculo-skeletal and central nervous systems (CNS). Within the CNS, EGR1 is known as an essential transcription factor involved in brain development. More specifically, EGR1 plays a role in how the early brain develops in response to environmental stimuli, formation of synapse architecture and certain types of memories. Many gene networks involved in growth and development rely on EGR1 to regulate functions such as synapse reformation after exposure to the environment. EGR1 is known to have numerous partners with whom it interacts to execute its functions. It is also involved in epigenetic regulation, which is a process by which genes are silenced or activated without changing DNA sequences in the genome. EGR1 may directly interact with TET1 to demethylate EGR1 target sites in the genome, and to increase gene transcription. In memory development, EGR1 plays a key role ensuring short-term auditory fear memory can be converted to long-term memory, and also ensures long-term spatial memory. In this study, our computational analyses suggest that EGR1 may interact with MEF2C. This work provides evidence of a protein-protein interaction of EGR1 and MEF2C in cultured cells and in the brain cortical areas of mice. Such an interaction may explain why these two genes regulate overlapped biological processes within the brain and sheds lights on how cascading events are initiated following neuronal stimulation.

Thesis (Ed. D.)--University of La Verne, 2003. / Includes bibliographical references (leaves 184-191).

Thesis (Ed. D.)--University of La Verne, 2003. / Includes bibliographical references (p. 184-191).