Matching Items (19)
Description
Prior research has established a relation between parenting behaviors and symptoms of child psychopathology, and this association may be influenced by both genetic and environmental factors. Gene-environment correlation, or the influence of a child’s genes on the environment they receive, represents one possible mechanism through which genes and environment combine to influence child outcomes. This study examined evocative gene-environment correlation in the relation between parenting and symptoms of child psychopathology in a sample of 676 twins (51.5% female, 58.5% Caucasian, 23.7% Hispanic/Latinx, primarily middle class, MAge=8.43, SD=.62) recruited from Arizona birth records. Using univariate ACE twin biometric models, genetic influences were found to moderately contribute to internalizing symptoms (A=.47, C=.25, E=.28), while externalizing (A=.86, E=.14) and ADHD (A=.84, E=.16) symptoms were found to be highly heritable. The genetic influences for positive (C=.54, E=.46) and negative (C=.44, E=.56) parenting were smaller and found to be nonsignificant. The correlations between parenting and types of psychopathology were examined and bivariate Cholesky decompositions were conducted for statistically significant correlations. Negative parenting was moderately positively correlated with externalizing and ADHD symptoms; the relation between externalizing symptoms and negative parenting was found to be due to shared genetics, whereas the relation between negative parenting and ADHD symptoms was due to the shared environment. The mixed results regarding the role of gene environment correlation in relations between parenting and child psychopathology indicate that further research on the mechanisms of this relation is needed.
ContributorsCarrizosa, Mya Grace (Author) / Lemery-Chalfant, Kathryn (Thesis director) / Corbin, William (Committee member) / Davis, Mary (Committee member) / Oro, Veronica (Committee member) / Department of Information Systems (Contributor) / Economics Program in CLAS (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
Description
Attention-deficit/hyperactivity disorder (ADHD) is a common developmental disorder characterized by symptoms of impulsivity, inattention, and hyperactivity that interfere with development. Given the lasting academic and social deficits associated with ADHD symptoms, it is critical to study the risk factors of this disorder and possible factors that could protect against its development. Therefore, the current study investigated the potential role of social support from parents, siblings, teachers, and peers as promotive and protective factors against the development of ADHD symptoms for children at familial risk of developing ADHD symptoms. Participants included 903 twins (30.5% monozygotic twins, 35.9% same-sex dizygotic twins, 31.7% opposite-sex dizygotic twins) from the longitudinal Arizona Twin Project. Children (51.6% female) were assessed for social support and ADHD symptoms at age 8 (M = 8.42, SD = 0.68) and for ADHD symptoms at age 9 (M = 9.71, SD = 0.93). Children’s familial risk for developing ADHD symptoms was assessed as a function of their cotwin’s symptom status at age 8 and the pair’s zygosity. Mixed model regression analyses indicated that familial risk was a robust predictor of ADHD symptoms. Further, peer acceptance was found to operate as a promotive factor against the development of ADHD symptoms, with some evidence for positive parenting as a promotive factor, as well. None of the forms of social support were found to be protective factors for children at familial risk of developing ADHD symptoms. Bivariate twin analyses revealed that peer acceptance and ADHD were related for both genetic and environmental reasons, suggesting that children’s heritable behaviors influence their peer acceptance. Future directions may include examining additional factors as possible moderators of familial risk of developing ADHD symptoms.
ContributorsHawkins, Jessica Kathryn (Author) / Lemery-Chalfant, Kathryn (Thesis director) / Miadich, Samantha (Committee member) / School of Life Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2020-12
Description
Hand-coding systems of measuring facial expressions were developed to study and analyze human emotions, but they are time-intensive and thus seldom used. As technology has advanced, new computer software programs, such as Affectiva, were developed to code facial expressions automatically using artificial intelligence and machine learning. Since this technology is still new, Affectiva and its validity remain understudied, and no psychological research has been conducted to compare Affectiva computer coding and hand coding of children’s emotions. The purpose of this study was to compare hand and computer coding of children’s expressions of emotion during a videotaped parent-child interaction. The study answered the following questions: 1) Do hand and computer coding agree?; and 2) Are hand and computer coding in higher agreement for some emotions than others? The sample included 25 pairs of twins from the Arizona Twin Project. Facial expressions were coded from videotape by a trained and reliable human coder and using the software Affectiva. The results showed that hand and computer coded emotion were in agreement for positive, but not negative emotions. Changing the context of the interaction to elicit more negative emotion, and using the same indicators of each emotion in computer and hand coding are suggested to improve the comparison of computer and hand coding.
ContributorsKwok, Connie (Author) / Lemery-Chalfant, Kathryn (Thesis director) / Davis, Mary (Committee member) / Miadich, Samantha (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
Asthma is one of the most common chronic diseases affecting children, and investigators have identified a number of risk factors that worsen asthma symptoms. Most prior studies have concluded that there is an association between one risk factor, poor sleep quality, and asthma; however, whether sleep quality predicts future asthma symptoms, asthma symptoms predict future sleep quality, or the relation is reciprocal is still unclear. The methodology of studies examining the asthma-sleep association has consisted of actigraphy and parent report to determine children's sleep duration and sleep efficiency, and lung function assessments with a spirometer on the participants to determine children's overall lung function. The purpose of the proposed study is to determine the strength of the cross-sectional and longitudinal associations between indicators of sleep quality and asthma. The proposed study plans to use a combination of actigraphy, sleep diaries, and lung function assessments using a spirometer to determine sleep quality and lung function, respectively. Future directions include determining the directionality of the association between sleep quality and asthma as well as strength of association.
ContributorsLacy, Kordell Reggie (Author) / Davis, Mary (Thesis director) / Miadich, Samantha (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-12
Description
Early childhood environment is critical to subsequent physical health in children and is influenced by children's primary caregivers \u2014 typically mothers. Maternal stress, one aspect of a child's environment, may shape the functioning of the child's physiological stress response system, which has been linked to later health outcomes, including pain. The current study evaluated whether: 1) early maternal stress, defined as maternal depressive symptoms and low socio-economic status, predicts later child pain; 2) early maternal stress relates to later child daily cortisol output; and 3) child's cortisol output across the day mediates the relation between early maternal stress and child pain. Maternal stress was assessed via questionnaires at twin age 12-months. At twin age seven years, twins' salivary cortisol was collected three times per day for three days. At twin age nine years, twins rated how often they experienced stomach, headache, and back pain weekly or more frequently. Results of multilevel linear and logistic regression analyses showed that early maternal stress did not predict later children's daily cortisol output or extent of child pain. Therefore, findings were inconsistent with the proposed mediation model. However, there was a marginally significant negative relation between child daily cortisol output and later extent of child pain. Current findings suggest that functioning of the stress response system, reflected in cortisol output, may have implications for the development of child pain. Future work evaluating intensely stressful early environments may provide clues about the links between a child's early environment and the development of his/her stress response system.
ContributorsRoth, Winter Rayne Nicole (Author) / Davis, Mary (Thesis director) / Miadich, Samantha (Committee member) / Department of Psychology (Contributor) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-12
Description
Alzheimer’s disease (AD) is characterized by the aberrant accumulation and aggregation of proteins that in turn contribute to learning and memory deficits. The mammalian target of rapamycin (mTOR) plays an essential role in regulating the synthesis and degradation of proteins that contribute to cell growth and learning and memory. Hyperactivity of mTOR can cause detrimental effects to protein homeostasis and has been linked to AD. The proline-rich Akt-substrate 40 kDa (PRAS40) is a negative regulator of mTOR, as it binds to mTOR directly, reducing its activity. Upon phosphorylation, PRAS40 detaches from mTOR thereby releasing its inhibitory effects. Increased phosphorylation of PRAS40, and a subsequent increase in mTOR activity has been linked to diabetes, cancer, and other conditions; however, PRAS40’s direct role in the pathogenesis of AD is still unclear. To investigate the role of PRAS40 in AD pathology, we generated a PRAS40 conditional knockout mouse model and, using a neuronal-specific Cre recombinase, selectively removed PRAS40 from APP/PS1 mice. Removing neuronal PRAS40 exacerbated Abeta levels and plaque load but paradoxically had no significant effects on mTOR signaling. Mechanistically, the increase in Abeta pathology was linked to a decrease in autophagy function. Our data highlight a primary role of PRAS40 in the pathogenesis of AD.
ContributorsSurendra, Likith (Author) / Oddo, Salvatore (Thesis director) / Velazquez, Ramon (Committee member) / Pratico, Domenico (Committee member) / School of Life Sciences (Contributor) / Dean, W.P. Carey School of Business (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
Description
The mammalian target of rapamycin (mTOR) is integral in regulating cell growth as it maintains a homeostatic balance of proteins by modulating their synthesis and degradation. In the brain, mTOR regulates protein-driven neuroplastic changes that modulate learning and memory. Nevertheless, upregulation of mTOR can cause detrimental effect in spatial memory and synaptic plasticity. The proline-rich Akt-substrate 40 kDa (PRAS40) is a key negative regulator of mTOR, as it binds mTOR and directly reduces its activity. To investigate the role of PRAS40 on learning and memory, we generated a transgenic mouse model in which we used the tetracycline-off system to regulate the expression of PRAS40 specifically in neurons of the hippocampus. After induction, we found that mice overexpressing PRAS40 performed better than control mice in the Morris Water Maze behavioral test. We further show that the improvement in memory was associated with a decrease in mTOR signaling, an increase in dendritic spines in hippocampal pyramidal neurons, and an increase in the levels of brain-derived neurotrophic factor (BDNF), a neurotrophin necessary for learning and memory. This is the first evidence that shows that increasing PRAS40 in the mouse brain enhances learning and memory deficits.
ContributorsSarette, Patrick William (Author) / Oddo, Salvatore (Thesis director) / Caccamo, Antonella (Committee member) / Kelleher, Raymond (Committee member) / School of Molecular Sciences (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
To date, it has been difficult to elucidate the role of tau in learning and memory during adulthood due to developmental compensation of other microtubule associated proteins in Tau knockout (KO) mice. Here, we generated an adeno-associated virus (AAV) expressing a doxycycline (doxy)-inducible short-hairpin (sh) RNA targeted to tau, and stereotaxically and bilaterally injected 7-month-old C57BL/6 mice with either the AAV-shRNAtau or an AAV expressing a scramble shRNA sequence. Seven days after the injections, all animals were administered doxy for thirty-five days to induce expression of shRNAs, after which they were tested in the open field, rotarod and Morris water maze (MWM) to assess anxiety like behavior, motor coordination and spatial reference memory, respectively. Our results show that reducing tau in the adult hippocampus produces significant impairments in motor coordination, endurance and spatial memory. Tissue analyses shows that tau knockdown reduces hippocampal dendritic spine density and the levels of BDNF and synaptophysin, two proteins involved in memory formation and plasticity. Our approach circumvents the developmental compensation issues observed in Tau KO models and shows that reducing tau levels during adulthood impairs cognition.
ContributorsTran, An Le (Author) / Oddo, Salvatore (Thesis director) / Velazquez, Ramon (Committee member) / Roberson, Erik (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Sibling interactions are natural contexts for learning about the appropriate expression of emotions. The emotionally charged nature of sibling interactions creates a convenient context to explore emotional reactivity and regulation. The purpose of this study was to examine the relations among parent-reported sibling relationship quality, observed sibling prosocial and antisocial behaviors displayed when playing a competitive marble game, and children's emotions coded from videotape. The sample consisted of 58 twin children who are currently participating in the longitudinal Arizona Twin Project. Parents completed the Sibling Relationship Questionnaire online at 5 and 8 years. Additionally, a competitive marble game interaction between the siblings took place in the home at 8 years and was videotaped for objective coding of prosocial, antisocial, and control behavior. Facial expressions were also coded from videotape using Emotient FACET software across the marble game interaction. Three mean composites of emotion were created, including positive and negative emotional facial expressions. Results showed that parent reported warmth did not predict the occurrence of positive emotions during the sibling interaction. However, siblings with high conflict showed less fear during the interaction. Parent reports of warmth predicted the extent to which siblings differed on emotion expression, however conflict did not. Parent ratings of conflict and warmth did not predict the extent to which the sibling dyad was emotionally intense. Findings regarding genetic and environmental effects were in line with previous reports of genetic influence on prosocial behavior and negative emotion, and expressions of joy being influenced by the environment. This study investigated noteworthy aspects of the sibling relationship that appear to promote children's adaptive development.
ContributorsGanase, Anaelle Shelina (Co-author) / Oro, Veronica (Co-author) / Roth, Winter (Co-author) / Doane, Leah (Co-author) / Lemery-Chalfant, Kathryn (Co-author, Thesis director) / Miadich, Samantha (Committee member) / Davis, Mary (Committee member) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
The aims of this project are: (i) to identify structural and molecular changes in the brains of 3xTg-AD mice and (ii) to determine whether decreasing S6K1 protects the brain from these changes. To achieve our goals, we decided to remove one copy of the S6K1 gene in 3xTg-AD mice by breeding them with S6K1 knockout mice (S6K1+/-). In previous studies, we have seen that reducing S6K1 levels in 3xTg-AD mice improved spatial memory and synaptic plasticity which was associated with reduced A and tau pathology. Here, we used a multiparametric MRI to assess volumetric and blood flow changes in the brain of 20-month-old 3xTg-AD mice. We found that 3xTg-AD/S6K1+/- mice had higher blood flow and cortical volume compared to 3xTg-AD mice. However, we saw no significant differences between 3xTg-AD mice and NonTg mice. We further found A levels and plaque numbers were significantly lower in 3xTg-AD/S6K1+/- mice compared to 3xTg-AD mice. This reduction in plaques could account for the improvement in blood flow in 3xTg-AD/S6K1+/- mice. To try to understand the reason behind the increase in cortical volume in the 3xTg-AD/S6K1+/- when compared to the 3xTg-AD, we measured markers of synaptic density, PSD95, and synaptophysin. We found that PSD95 levels were not different between the four groups. However, synaptophysin levels were significantly lower in 3xTg-AD mice compared to NonTg levels and returned to baseline levels in 3xTg-AD mice lacking one copy of the S6K1 gene. This difference in synaptophysin could explain, at least in part, the difference in volume between the four groups analyzed. Overall, this represents the first evidence showing that reducing mTOR signaling improves blood flow and cortical volume in a mouse model of AD.
ContributorsShukla, Prakriti (Author) / Oddo, Salvatore (Thesis director) / Caccamo, Antonella (Committee member) / Jankowsky, Joanna (Committee member) / School of Molecular Sciences (Contributor) / School of Public Affairs (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05