Melbourne School of Psychological Sciences - Theses
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ItemAdolescent-onset depression: the interplay between family relationships, brain development and inflammation( 2014)Adolescence is an important life phase in which to explore psychological functioning. The emergence of depression during adolescence has been linked to aspects of both the family environment and brain developmental processes, although few studies have explored these two key variables together to prospectively determine adolescent vulnerability to depression. Consequently, the aim of the present thesis was to determine whether volume change in the pre-frontal cortex (PFC), amygdala and hippocampus partially, but significantly, mediate the effects of maternal behaviours on the onset of depression during adolescence. A secondary aim of this study was to explore a specific mechanism through which these changes in the brain may occur; specifically, systemic inflammation as marked via the production of CReactive Protein (CRP). Overall, it was expected that family interactions charaterised by higher rates and longer durations of Aggressive and Dysphoric maternal behaviours would predict the onset of clinical depression. Moreover, it was hypothesized that such maternal behaviours would predict changes in brain volume previously reported in depressed samples, as well as increased levels of CRP. Lastly, it was anticipated that elevated levels of CRP associated with more hostile maternal behaviours would partially, but significantly, mediate the relationship between parenting and structural brain development. Data from the larger Adolescent Development Study (ADS) were used to explore these aims and hypotheses. The ADS is a prospective longitudinal research study that consists of four waves of data collection, with data for this research project drawing on each of these four data collection time points in the following areas; magnetic resonance imaging (MRI) (T1, T3 and T4), family interaction tasks (T1), diagnostic assessment of mental health (T1 -T4) and saliva samples to measure inflammation (T2). As such, participants in this research comprised a smaller sub-sample of the total ADS sample population. This sub-sample consisted of N = 160 adolescents (females = 80), of which N = 32 (females = 22) received a diagnosis of clinical MDD. Path analysis techniques were used to analyse the data. The findings from the present study confirmed that maternal behaviours and changes in brain volume over time both increase vulnerability to MDD onset during adolescence. However, no evidence was found that changes in brain volume across the ages of 12 to 19 years in the PFC, amygdala or hippocampus mediated the effects of these maternal behaviours on mental health outcomes. Moreover, maternal behaviours were also found to result in detectable changes in brain volume over time, highlighting how even subtle variations in parenting behaviour influences biological development. However, when the immune system was included in these analyses, results suggested that CRP did not mediate the influence of maternal behaviours on these structural changes in the brain. The complexities of these interactions and their implications for our understanding of etiological models of depression during adolescence are considered.
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ItemDepression and immunity in adolescents: early precursors to disease?( 2012)Inflammation and immune dysfunction have been proposed to be mechanisms relevant to clinical depression. However, research on this topic is limited by the paucity of lifespan and longitudinal studies, making it difficult to address causality. This project aimed to examine inflammatory and depressive measures in adolescents from the community using both cross-sectional and prospective longitudinal designs. Experiment 1 was a cross-sectional, two-group study of 13 clinically depressed adolescents aged 13-18 years (11 females), and 13 age- and sex-matched healthy controls, both recruited from the community. Sixteen cytokines were measured in saliva and serum. Depressed adolescents displayed significantly elevated levels of C-reactive protein (CRP), Haptoglobin, Serum Amyloid P (SAP), and Alpha-2-macroglobulin (A2M) in saliva compared to controls, but not in serum, or for any other cytokine. Depressed adolescents also did not display a higher ratio of T helper cell 1- to T helper cell 2-type cytokines compared to controls. Experiment 2 was a prospective study of 67 adolescents (27 females) followed from 12-18 years of age and recruited from the community. Self-report depressive symptoms measured by the Center for Epidemiological Studies Depression Scale (CES-D) and Axis-I psychopathology measured by The Schedule for Affective Disorder and Schizophrenia for School-age Children (KSADS) were measured at four phases, and four salivary acute-phase proteins (CRP, Haptoglobin, SAP, and A2M) were measured at Phase II. Temperamental negative emotionality (NEM) was also assessed at age 12. Results showed that elevated CRP was significantly correlated with elevated CES-D scores cross-sectionally, but no inflammatory markers predicted the onset of a depressive illness or an increase in depressive symptoms over time. There was a significant Sex x CRP interaction effect on CES-D measured at Phase I, II, and IV, with a relationship between CRP and CES-D only apparent for females. Examining only females demonstrated significant associations between CRP and CES-D at all four phases, including CES-D measured two years prior to inflammation, suggesting that for females, depressive symptoms may precede elevated levels of CRP, however, further longitudinal research is required that measures inflammation at more than one time point. At Phase II, there were significant interactions of NEM temperament x CRP on CES-D, with a relationship between CRP and CES-D only for those with a high NEM score. Post-hoc analyses showed that body mass index (BMI) was also a significant moderator of the relationship between CRP and CES-D at Phase II, with a stronger association for participants with a higher BMI score. Measures of early-life stress and childhood trauma were not associated with inflammatory markers. These results suggest that salivary CRP is a marker of adolescent depression, but levels of this inflammatory marker do not predict the development of depressive illness. The results, along with other research, suggest that depressive symptoms may be a risk factor for chronic inflammation and associated medical diseases, especially for females. Furthermore, obesity may be another consequence of depression which can lead to this observed elevated inflammation. Finally, sex hormones should be considered in models of depression, obesity, and inflammation.