Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (p. [188]-213).

Thesis (Ph. D.)--Ohio State University, 2005. / Title from first page of PDF file. Document formatted into pages; contains xii, 117 p.; also includes graphics (some col.) Includes bibliographical references (p. 74-81). Available online via OhioLINK's ETD Center

Dissertation (Ph.D.) - Simon Fraser University, 2005. / Dissertation (Dept. of Psychology) / Simon Fraser University. Includes bibliographical references (leaves 86-93).

ABSTRACT Seasonal affective disorder (SAD) is characterized by annual recurrence of clinical depression in the fall and winter months. The importance of SAD as a public health problem is underscored by its high prevalence (an estimated 5%) and by the large amount of time individuals with SAD are impaired (on average, 5 months each year). The specific cause of SAD remains unknown; however, researchers have identified possible chronobiological and psychological vulnerabilities to SAD. The study aimed to clarify psychological and chronobiological correlates of SAD in the first test of an integrative model of SAD. The project used a longitudinal design to test the respective contributions of the chronobiological and cognitive vulnerabilities on winter depression severity in 31 SAD patients and 33 never-depressed controls at sites in Burlington, VT and Pittsburgh, PA. The measures selected for the cognitive vulnerability were established measures of vulnerability to nonseasonal depression with empirical support for their relevance to SAD: brooding rumination, dysfunctional attitudes, cognitive reactivity to an induced sad mood, and season-specific cognitions. The chronobiological vulnerability was measured as Phase Angle Difference (PAD) and deviation from PAD of 6 hours. All measures were completed once in the summer, when the SAD patients were remitted, and once in the winter, when patients were clinically depressed. Patients were distinguished from controls on most cognitive vulnerability measures (brooding, as well as rumination, dysfunctional attitudes, and seasonal beliefs). SAD patients exhibited shorter PAD than controls, but did not exhibit greater deviation from PAD-6. Results provide further support for specific cognitive, but not chronobiological, vulnerabilities in prediction of SAD. Limitations of the current sample are discussed. Results hold implications for future SAD research bridging the chronobiological and psychological disciplines with the ultimate aim of improved understanding, assessment, treatment, and prevention of SAD.

Not available / text

Thesis (M.A.)--York University, 2007. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 53-72). 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:MR38808

Thesis (Ph.D.) in Psychology--University of Maine, 2003. / Includes vita. Includes bibliographical references (leaves 117-135).

No description available.

1H-Magnetic Resonance Spectroscopy (MRS) is a MRI paradigm that allows the levels of specific metabolites to be estimated in vivo [1]. This means that insights into the biochemical changes associated with a rare genetic change that raises the risk of mental disorders, and the impact of having a mental disorder, can potentially be made. In this study the levels of glutamate and N-acetyl-aspartate (NAA) were measured at 3T field strength in three separate voxels: right dorsolateral prefrontal cortex (DLPFC), left DLPFC and the anterior cingulate cortex (ACC). This thesis reports that members of a family that carry a unique t(1;11)(q42.2;q14) translocation that affects DISC1 have a substantially raised risk of developing a range of mental disorders, including bipolar affective disorder, schizophrenia and depression. A genetic change that leads to an increase in the susceptibility to a range of mental disorders is in line with other genetic studies that have been recently reported [2, 3]. The translocation was associated with a significant reduction in right DLPFC glutamate (mean difference= -2.11, CI= -0.24: -3.98, p=0.029) and left DLPFC NAA (mean difference= -1.97, CI= -0.34: -3.61, p=0.020). Changes in these metabolites offer some support to studies in cells and rodents trying to understand the impact of the t(1;11) translocation. More specifically the results offer support to studies that have linked alterations in DISC1's molecular biology to changes in glutamate receptors and mitochondrial function [4-6]. The results need to be interpreted with some caution due to the small sample size and the lack of a significant effect in the bilateral DLPFCs. People with a major mental disorder were also found to have significantly lower levels of glutamate in the left DLPFC (F=3.16, p=0.047). When compared to controls the reductions were significant in the people with a diagnosis of schizophrenia (mean difference= -0.86, CI= -0.19: -1.51, p=0.012), but not in people with bipolar affective disorder. Glutamate levels were significantly correlated with negative symptoms in people with schizophrenia (SANS r= -0.44, CI= -0.07: - 0.70, p= 0.024). The effect of experiencing depressive symptoms was also evaluated due to support for a link in previous studies [7, 8]. Whist the participants were not recruited due their experience of depressive symptoms, metabolite levels were found to be significantly associated with depressive symptoms in all participants with a mental disorder (all three voxels, both NAA and glutamate p < 0.05). The experience of depressive symptoms is not the same experiencing a depressive episode though, and further work may offer more insights into the association between metabolite changes and experience of depression. These findings provide insights into the relationship between diagnosis, current psychopathology and genetic risk in major mental disorders. The thesis provides some support that MRS imaging can be used to try understand neurobiological changes that are associated a genetic change, which is in turn linked to range of mental disorders. Interpreting the results of MRS imaging studies in humans remains challenging due to the complexity of the molecular biology that underpins the estimated metabolite levels, but where there has been a wide range of translational study into a specific protein (or genetic change) MRS may offer further information to help understand any effect in vivo.

Augmenting/reducing of the evoked potential has been shown to be related to sensation seeking (SS) and specific clinical disorders. Buchsbaum demonstrated that patients with bipolar affective disorders (BAD) tend to be augmenters, as is the case with sensation seekers, and patients with unipolar affective disorders (UPD) tend to be reducers. In addition, he reported that prophylactic medication reduced the tendency to augment in bipolar patients. However, evidence for these relations is restricted to a few studies. This study explores whether Buchsbaum’s initial findings can be found in a naturalistic clinical setting. Acoustic evoked potentials were recorded for six levels of intensity (59, 71, 79, 88, 92, 96 dB SPL) from 24 healthy adults, 21 unipolar depressed patients, and 21 patients with BAD. Participants also completed personality questionnaires, especially the Sensation Seeking Scales Form V. Results revealed a positive correlation between SS and augmenting/reducing in healthy controls, thereby replicating earlier findings. Bipolar depressed patients showed larger P1/N1 slopes than healthy controls, when medication was statistically controlled. Unipolar depressed patients showed smaller P2 slopes, but only when medication was not controlled. Implications of these results for further research on augmenting/reducing and affective disorders and their relationship to SS are discussed. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.