Photocopy of typescript. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1979. / Bibliography: leaves 50-56. / Microfiche. / vii, 56 leaves ill. 28 cm

Typescript. / Thesis (Ph. D.)--University of Hawaii, 1969. / Bibliography: leaves [105]-109. / iii, 109 l illus., graphs, tables

Typescript. / Binder's title: Intellectual abilities of Filipino sixth grade students. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1973. / Bibliography: leaves 176-187. / viii, 301 l illus., tables

Cognitive deficits are a hallmark feature of both Down Syndrome (DS) and Alzheimer's Disease (AD). Individuals with DS exhibit a very early onset of AD neuropathology, byt heir mid to late 30's. Extra copies of the genes on chromosome 21 may play an important role in this accelerated onset of AD in DS individuals. The amyloid precursor protein (APP) is located on chromosome 21, and among its cleavage products is amyloid-beta (Aß), a component of amyloid plaques. The presence of Aß and amyloid in the brain is a key pathogenic factor, and is considered the central and causative neuropathology in AD by the amyloid cascade hypothesis. Growing evidence suggests an important role for cholesterol in the pathogenesis of AD, particularly in APP metabolism and production of A peptides. The ATP-Binding Cassette-G1 (ABCG1) transporter is located on chromsome 21, and is believed to participate in the maintenance of cholesterol homeostasis. The effects of ABCG1 expression on the production of Aß have proved inconclusive in in vitro studies, demanding an in vivo resolution where appropriate physiology is maintained. To test the hypothesis that overexpression of ABCG1 will accelerate the onset or progression of AD in vivo, we evaluated the cognitive performance of ABCG1-overexpressing mice before and after crossing to the PDAPP mouse model of AD. Both normal and AD mice overexpressing ABCG1 showed no significant deficits on several cognitive tests, including reference and working memory task variations of the Morris Water Maze. Golgi analysis of neuronal structure revealed significantly reduced dendritic complexity in both normal and PDAPP mice overexpressing ABCG1, suggesting that the cholesterol-related functions of ABCG1 have a potentially important role in dendrite development. Interestingly, behavioural analysis of ABCG1-deficient mice revealed a gene-dose dependent trend toward worsened performance on the water maze probe trial, suggesting that the pathways that may compensate for ABCG1 overexpression could be unable to offset a complete deficiency. These experiments suggest an important role for ABCG1 in maintaining cellular cholesterol homeostasis, but do not support the hypothesis that ABCG 1 expression contributes to the accelerated onset of AD pathology in DS individuals.

A substantial amount of research has investigated the psychophysiological profiles of various mood and emotional states; however, very little research has investigated individuals� mood responses from a psychophysiological perspective. As a result, little is known about the psychophysiological reactivity of individuals to various mood-related responses, or the ability of psychophysiological measures to differentiate between response styles. Furthermore, most investigations in the area of mood-related response styles have relied on participants self-report responses of their mood reactivity, which is considered to be susceptible to demand characteristics and response bias. Psychophysiological measures are thought to offer a unique and alternative measure of mood reactivity that can corroborate, or challenge self-report findings. They are considered to be less susceptible to demand effects than self-report, and can detect subtle changes in mood reactivity activity when an overt response is not apparent. In view of this, the primary objective of this thesis was to move beyond a reliance on subjective self-report measurements of mood reactivity, and to investigate the consequences of depressed mood-related cognitive response styles from a psychophysiological perspective. As part of this investigation, this thesis aims to address a number of theoretical and practical questions relating to the use of psychophysiological measures in mood research and clinical practice. The research is divided into four studies, each one focusing on a particular aspect of the investigation. The aim of Study 1 was to select and trial a laboratory-based mood induction procedure (MIP) and a self-report mood measure, with the intention of developing a reliable method of inducing and measuring depressed mood. Two film clips that contained either positive or negative affective content were presented to participants. Self-report responses on the Mood Scale confirmed that the negative film clip elicited a very unpleasant mood state with high emotional arousal, and that the positive film clip elicited a mildly pleasant mood state with low emotional arousal. The positive and negative Film Clip MIPs were then used in Studies 2 and 2a, to investigate participants� psychophysiological reactivity to induced mood. The aim of Studies 2 and 2a was to identify a set of psychophysiological measures that would differentiate between participants� mood states. In Study 2, the positive and negative Film Clip MIPs, from Study 1, were again presented to participants. Corrugator supercilii facial EMG activity, zygomaticus major facial EMG activity, skin conductance activity (SCA), heart rate (plethysmograph, sphygmomanometer), systolic blood pressure, diastolic blood pressure, and self-report ratings on the Mood Scale were recorded. Results confirmed that participant self-reported affective responses were similar to those reported in Study 1; however, mixed results were obtained in regards to individuals� psychophysiological responses to the MIPs. Facial EMG activity and heart rate (plethysmograph) were consistent with participants� self-reported mood, whereas, SCA and systolic blood pressure were inconsistent with participants� self-reported mood. Diastolic blood pressure and heart rate (sphygmomanometer) did not differentiate between the MIPs. As the results were somewhat contradictory to expectations, it was decided to further investigate the psychophysiology of induced mood in Study 2a, using a revised set of psychophysiological measures. In Study 2a, the positive and negative Film Clip MIPs were again presented to participants. Corrugator supercilii facial EMG activity, zygomaticus major facial EMG activity, SCA, heart rate (ECG), and finger temperature, were recorded along with participants� Mood Scale ratings. It was found that facial EMG activity and SCA, paralleled participant self-report as expected, and were most responsive to participants� change in mood state. Heart rate (ECG) and finger temperature did not clearly differentiate between the induced mood states. The aim of Study 3 was to conduct an experimental, laboratory-based investigation, into the psychophysiological and subjective mood consequences of two cognitive response styles: self-focused depressive rumination and external-focused distraction. As in the previous study, the negative Film Clip MIP and the Mood Scale were used to induce depressed mood and to measure participants� subjective mood state. Psychophysiological reactivity was recorded by measuring participants� corrugator supercilii facial EMG, zygomaticus major facial EMG, SCA, heart rate (sphygmomanometer), systolic blood pressure, and diastolic blood pressure. Trait response style was measured using the Response Style Questionnaire (RSQ; Nolen-Hoeksema & Morrow, 1991) and social desirability was measured using the Marlowe Crowne-Social Desirability Scale (MC-SDS; Crowne & Marlowe, 1960). As predicted by the Response Style Theory of depression (RST), increased self-reported negative mood was found when participants responded to the induced depressed mood, using a self-focused depressive rumination response style, rather than an external-focused distraction response style. Psychophysiological activity increased over the course of the negative Film Clip MIP for all psychophysiological measures, however, only corrugator supercilii facial EMG activity clearly differentiated between the cognitive response styles, in a way predicted by individuals� self-report responses. There was no evidence of a relationship between participants� trait response style and their psychophysiological reactivity or mood responses during the experiment. However, individuals high in trait rumination reported greater depressive symptomatology, and less mood reactivity during the experiment, than those high in trait distraction. Furthermore, participants� ratings of social desirability were positively associated with their level of depressive symptomatology and trait rumination. The aim of Study 4 was to conduct a pilot study to investigate the psychophysiological consequences of two further cognitive response styles: negative automatic thoughts and positive autobiographical recall. A series of twelve single-case (ABC-ABC) experiments were carried out using a procedure analogous to a clinical therapy process. Initially a depressed Story MIP was used to induce a depressed mood in participants (A). Participants were then required to respond to their depressed mood using negative self-statements (B), and positive autobiographical recall (C). Consistent with previous studies, zygomaticus major facial EMG and corrugator supercilii facial EMG clearly paralleled participants� mood reactivity throughout the experiment, whereas SCA and heart rate showed less consistent patterns of reactivity. This thesis has made an important contribution to mood and psychophysiological research by presenting the first in-depth investigation into the psychophysiological consequences of how people respond to depressed mood, from both a theoretical and a clinical perspective. It is anticipated that the findings of this research will bring about further investigation into the comparative efficacy of various brief mood-related cognitive intervention techniques, which will ultimately assist scientist-practitioners in selecting suitable brief cognitive intervention techniques for helping clients ameliorate their negative mood, emotional, and cognitive states.

Typescript (photocopy) / Appendix, 26 leaves, in end pocket / xix, 497 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.) Dept. of Psychology, University of Adelaide, 1983

Thesis (Ph.D.)--York University, 2005. Graduate Programme in Philosophy. / Typescript. Includes bibliographical references (leaves 197-218). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR11620

Thesis (Ph.D.)--University of North Carolina at Greensboro, 2007. / Title from PDF t.p. (viewed Mar. 3, 2008). Directed by Robert E. Guttentag; submitted to the Dept. of Psychology. Includes bibliographical references (p. 50-52).

Thesis (Ph. D.)--University of Adelaide, 1985. / Includes bibliographical references (leaves 388-403).

Thesis (Ph. D.)--University of Adelaide, 1985. / Includes bibliographical references (leaves 347-361).