UMD Theses and Dissertations
Permanent URI for this collectionhttp://hdl.handle.net/1903/3
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Item Early emotional caregiving environment and associations with memory performance and hippocampal volume in adolescents with prenatal drug exposure(2023) Kohn, Brooke Hannah; Riggins, Tracy; Psychology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Early adversities, including prenatal drug exposure (PDE) and a negative postnatal emotional caregiving environment, impact children’s long-term development. The protracted developmental course of memory and its underlying neural systems offer a valuable framework for understanding the longitudinal associations of pre- and postnatal factors on children with PDE. This study longitudinally examines memory and hippocampal development in 69 parent-child dyads with PDE histories to investigate how the early emotional caregiving environment affects children with PDE’s neural and cognitive systems. Measures of physical health, drug exposure, and the emotional caregiving environment were collected between 0-24 months. At age 14 years, adolescents (N=69, 52.17% Female) completed multiple measures of episodic memory. at ages 14 (n=27) and 18 (n=17) years, a subset of adolescents underwent magnetic resonance imaging (MRI) scans. Latent constructs of episodic memory and the caregiving environment were created using Confirmatory Factor Analysis. Multiple regressions revealed a negative emotional caregiving environment during infancy was associated with poor memory performance and smaller left hippocampal volumes at 14 years. Better memory performance at 14 years predicted larger right hippocampal volume at 18 years. At 18 years, the association between the emotional caregiving environment and hippocampal volume was moderated by sex, such that a negative emotional caregiving environment was associated with larger left hippocampal volumes in males but not females. Findings suggest that the postnatal caregiving environment may modulate the effects of PDE across development, influencing neurocognitive development.Item ACUTE EXERCISE INDUCED MICROSTRUCTURAL AND FUNCTIONAL CHANGES IN THE HIPPOCAMPUS OF OLDER ADULTS(2023) Callow, Daniel; Carson, Jerome J; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Declining memory function is a common complaint of aging adults and a primary symptom of mild cognitive impairment (MCI) and Alzheimer’s disease (AD). The hippocampus is often the first brain area to exhibit noticeable deficits in age and pathologically-related cognitive decline and is a necessary structure for proper memory function. More specifically, the dentate gyrus (DG) and the third cornu ammonis area (CA3) of the hippocampus directly support mnemonic discrimination (MD), which is the process of reducing interference among new representations and distinctly encoding them as independent memories. Poor MD is associated with age and is a presymptomatic biomarker of cognitive decline and is believed to result from reduced neurogenesis, angiogenesis, and synaptogenesis within the DG/CA3 subregion of the hippocampus. While causes and treatments for memory decline remain elusive, lifestyle interventions, especially physical activity, have received attention as cost-effective and safe means of ameliorating and potentially preventing cognitive decline in a growing aging population. Animal and human studies suggest exercise benefits the hippocampal structure, preserving neurogenesis and angiogenesis in aging rodents and macrostructure and memory in older adults. However, the mechanisms by which exercise affects the human hippocampus remains a significant knowledge gap in the field and is a critical aspect in understanding the long-term impact exercise has on the aging hippocampus. To better address this gap, researchers have begun implementing acute exercise studies, which allow for greater control of non-exercise-related factors, are cheaper and more time efficient to conduct than training studies, and can predict and inform training-related adaptations. Unfortunately, limitations in the study designs, population tested, specificity of cognitive tasks, and spatial resolution of human imaging techniques have posed significant barriers to our understanding of how acute exercise relates to healthy brain aging at the functional and microstructural levels. Therefore, the objective of this dissertation was to expand our understanding of how acute aerobic exercise alters the function and microstructure of the aging hippocampus. Three within-subject studies were conducted comparing the relationship between a 30-minute bout of moderate to vigorous intensity aerobic exercise vs seated rest on MD performance, hippocampal microstructure, and high-resolution hippocampal-subfield microstructure and functional activity in healthy older adults. In study one, acute exercise preserved MD performance compared to decrements exhibited after seated rest in a pre and post-condition study design. In study two, a post-condition-only study design, acute exercise elevated microstructural diffusion within the hippocampus, indicative of a hippocampal neuroinflammatory response and upregulation of neurotrophic factors. Finally, in study three, a post-condition-only study design, we found that acute exercise resulted in lower MD, suppressed MD-related DG/CA3 network hyperactivity (indicative of healthier network function), and led to higher DG/CA3 extracellular diffusion. However, these neuroimaging-based correlates of hippocampal neuroplasticity and network function were not associated with differences in MD performance. These findings suggest that higher-intensity acute exercise can alter memory performance and stimulate neuroplasticity and neurotrophic cascades within the hippocampus and the DG/CA3 subfield, potentially via different mechanisms. Furthermore these results give insight into the immediate neurotrophic and behavioral effects of acute moderate to vigorous intensity aerobic exercise in older adults and provide new methods and tools for better understanding if and how exercise promotes healthy brain aging. Finally, these initial findings lay a foundation for optimizing exercise prescription and identifying future effective exercise treatments.Item PARENT PERSPECTIVES ON DIAGNOSIS OF AND SERVICES FOR CHILDREN WITH CORTICAL VISUAL IMPAIRMENT(2019) Kempler, Sara Kathleen; Beckman, Paula J; Special Education; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Medical advances in recent years have increased survival rates of infants born prematurely and/or infants and children that present with life-threatening conditions (Good et al., 1994; Khetpal & Donahue, 2007; Murphy & Carbone, 2011). These increased survival rates are associated with an increase in the number of children who have severe and/or multiple disabilities, including those conditions that are associated with cortical visual impairment. Children with typical or nearly typical eye exams, but having observable visual impairment are those generally diagnosed with cortical visual impairment, or CVI (Jan, Groenveld, Sykanda, & Hoyt, 1987). Delayed or lack of diagnosis of CVI can lead to missed opportunities for learning, and especially missed sensitive periods during which recovery can occur faster (Hubel & Wiesel, 1970; Roman-Lantzy, 2018). Without diagnosis, children may not be eligible for funding assistance for educational materials (American Printing House for the Blind, n.d.b). The purpose of this study was to explore parents’ experiences in getting a diagnosis of CVI for their children. For example, whether there were lapses in time between suspected vision difficulties and diagnosis, and what information was provided when diagnosis was obtained. The research questions guiding this investigation included: What are parents’ experiences in seeking a diagnosis for their child’s suspected vision challenges? What needs do parents recall related to information and supports while seeking a diagnosis for their child’s suspected vision challenges? What kind of information is offered or readily available to parents upon diagnosis of CVI? The primary data source for this study was interviews with parents of children having diagnosed CVI. Secondary data sources included interviews with ophthalmologists, teachers of the visually impaired, and records review.Item CHARACTERIZATION OF CHRONIC MONOCULAR DEPRIVATION AND ESTROGEN ADMINISTRATION IN ADULT RODENTS(2018) Sengupta, Deepali Clare; Quinlan, Elizabeth M; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Reduced synaptic plasticity and excitatory synapse density contribute to age-related cognitive decline, and constrain recovery of function from injury in adults. A parallel reduction in circulating sex hormones in both sexes, particularly estrogens, exacerbates this decline in synaptic plasticity. Conversely, estrogen therapy in aged members of many species restores synapse density, promotes synaptic plasticity, and improves learning/memory. Importantly, acute estrogen administration can promote rapid synaptogenesis, and these new synapses can be stabilized by activity. Here I ask if estrogen treatment can promote synaptic plasticity in the primary visual cortex (V1) of aged rats. I demonstrate robust expression of estrogen receptors (ERs) in V1 of adult male and female rats, suggesting an opportunity to enhance plasticity with estrogens. I test this hypothesis following the induction of amblyopia by chronic monocular deprivation (cMD). I show that cMD reduces thalamic innervation from the deprived eye, and increases molecular markers which constrain plasticity, consistent with observations that the deficits induced by cMD are highly resistant to reversal. Surprisingly, cMD did not change markers for excitatory synapses, suggesting a homeostatic increase in synapses serving the non-deprived eye (NDE) to maintain synaptic density within an optimal range. Importantly, visually-evoked potentials (VEPs) induced by repetitive visual stimulation to the deprived eye depress more rapidly than those of the NDE, consistent with cMD inducing an increase in the probability of neurotransmitter release (Pr) at synapses in the cMD pathway. In contrast, treatment of cMD adults with a single dose of 17α estradiol significantly increased markers for excitatory synapses, and estradiol treatment followed by visual stimulation also increased markers for excitatory synapse activity. Repetitive estradiol treatments increased excitatory synapse markers, but not synaptic activity markers. Furthermore, one dose of estradiol enhanced VEP amplitude following repetitive visual stimulation, however this was observed only in response to stimulation of the NDE. As presynaptic ERs are known to increase Pr at glutamatergic synapses, this suggests that the effects of estradiol are specific to spared synapses where Pr has not been up-regulated by deprivation. Exploiting this selectivity may allow for receptive field remapping of spared inputs around a scotoma or cortical infarctItem FUNCTIONAL CONNECTIVITY PATTERNS ASSOCIATED WITH AGING, PHYSICAL ACTIVITY, AND GENETIC RISK FOR ALZHEIMER’S DISEASE IN HEALTHY HUMAN BRAIN NETWORKS.(2017) Chirles, Theresa Jeanne; Smith, Carson J; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Leisure time physical activity (PA) and exercise training help to improve and maintain cognitive function in healthy older adults and in adults with the APOE-ε4 allele, a genetic risk for Alzheimer’s Disease (AD). Earlier work finding increased functional connectivity in the Default Mode Network (DMN) after a 12-week walking intervention in 16 older adults with mild cognitive impairment is presented in Chapter 3. The primary dissertation study investigating differences in brain function depending on PA level and genetic risk for AD prior to changes in cognition is presented in Chapters 4-6. Useable resting state and anatomical MRI scans were collected from 69 healthy adults (22-51 years) as well as saliva for APOE genotyping (carriers defined as homozygotes or heterozygotes of the ɛ4 allele) and responses to the Paffenbarger Physical Activity Questionnaire (High PA >1500 kcal, Low PA <1500 kcal per week). The following network measures of functional connectivity were calculated: global efficiency; node strength of Default Mode Network (DMN) and Fronto-Parietal Network (FPN) hubs and hippocampal subsections; and long-range connectivity of the medial prefrontal cortex (mPFC) and posterior cingulate cortex (PCC) in the DMN. Multiple linear regression analysis revealed statistically significant results for the long-range connectivity of the left PCC, a prominent hub of the DMN, and left mPFC. The differences in projected trajectories of the connectivity are potentially reflective of the compensatory time-course in our participants based on interactions of PA level and APOE status. The Low PA non-carriers had a positive slope indicating increased connectivity with age while carriers and non-carriers in the High PA category had horizontal aging trajectories. PA is associated with cognitive reserve (CR), a term describing the protection and adaptation of cognitive processes through neural efficiency and compensation mechanisms, and it is possible the Low PA non-carriers exhibited compensatory increases in connectivity of the left mPFC-PCC earlier than High PA study participants due to lower levels of CR. The promising findings that rs-fMRI can be used as an early detection of brain changes sensitive to PA levels and APOE-ɛ4 status are critical to the research and treatment of AD.Item Elements of Employment Related Disclosure of Disability after Brain Injury(2012) Burnhill, David Asher; Fabian, Ellen; Counseling and Personnel Services; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Few studies have examined the elements of disclosing a disability in the workplace. Those few studies had a primary focus on reasonable accommodations (RA) where the disclosure process was either secondary or tertiary to the study. Further, there have been no studies to date which have examined elements of disclosure for individuals with brain injury (BI). Disclosure of disability is a crucial first step in the request process for a reasonable accommodation in the workplace and is required by the ADA for individuals requesting job related accommodations. This study examined the (a) experiences of work-related disability disclosure for individuals with BI, (b) the injury, demographic and other factors associated with the decision to disclose a disability at work, and (c) employment-related outcomes associated with disclosure. The primary goal of the current study is to describe the population of people with brain injury who disclose their disability in the workplace and to make inferences about the contributing factors involved in the disclosure process. The study used a cross-sectional survey methods research design. The study consisted of 200 individuals recruited from an online survey hosted on the Brain Injury Association of America's website. Of these participants, 144 (74.6%) disclosed their disability on at least one job and 91 (45%) were currently working. Level of education (X2 =11.945, 3, p=.008), self-efficacy score (F=7.52; p=.007) and time between injury and current age (F=4.56; p=.034) were significantly related to disclosure. Logistic regression analyses were used to examine the combined effects of several predictor variables with disclosure. In this analysis, only time since injury and self-efficacy (SE) scores were significant, where higher SE scores increased the odds of disclosure, and time since injury decreases the odds of disclosure (the more recent the injury, the more likely the individual was to disclose).Item The Gonadotropin Releasing Hormone-3 System in Zebrafish: Early Development and Regulation(2008-12-15) Abraham, Eytan; Zohar, Yonathan; Marine-Estuarine-Environmental Sciences; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)The objective of this study was to expand our understanding of the early development of forebrain Gonadotropin Releasing Hormone (GnRH) neurons in vertebrates in general and in fish in particular. The correct migration during early development of the hypophysiotropic GnRH neurons from the olfactory region to the hypothalamus is crucial for normal gonadal development and reproduction. We developed a Tg(GnRH3:EGFP) zebrafish line in which EGFP is specifically expressed in GnRH3 neurons. Using this line, we have studied in detail the early spatiotemporal development of the GnRH3 system in vivo. In addition, we have studied various factors, including GnRH3, Netrins and Hedgehog to better understand some of the mechanisms that mediate this complex axophilic neuron migration event. Lastly, we have conducted targeted GnRH3 neuron ablation experiments in view of determining the embryonic origin of POA-hypothalamic GnRH3 neurons and the effect of lack of GnRH3 neurons in the CNS. Our findings show that: 1) GnRH neurons first differentiate and express GnRH3 at 24-26 hours post fertilization (hpf) and immediately thereafter begin to extend fibers. 2) GnRH3 neurons project a complex network of fibers, prior the GnRH3 soma migration, to various CNS regions, and to the pituitary. 3) GnRH3 soma begin migrating towards the hypothalamus at 3 days post fertilization (dpf), passing through the terminal nerve (TN), lateral telencephalon, and reaching the hypothalamus by 12 dpf. 4) expression of GnRH3 itself is necessary for the normal early differentiation and fiber extensions of GnRH3 neurons. 5) Netrin1a is directly involved as a chemoattractant in GnRH3 fiber organization and subsequently, in GnRH3 soma migration to the hypothalamus. 6). Netrin2 is required for normal early ZF embryogenesis. 7). Sonic hedgehog a does not serve as a specific factor in the development of the GnRH3 system. 8). GnRH3 neuron regeneration capacity is temporally limited. 9). Successful ablation of olfactory GnRH3 neurons during development results in lack of GnRH3 neurons in the entire sexually mature brain as well as abnormal gonadal development and inability to reproduce. This study expands our understanding vis-à-vis the early events that occur during GnRH3 system development and that regulate this complex process. In a broader sense these findings augment current knowledge regarding the regulation of long range tangential neuron migration during development.