Adolescent-onset depression: the interplay between family relationships, brain development and inflammation
AuthorJackson, Jennifer Sun-Fah
AffiliationMelbourne School of Psychological Sciences
Document TypePhD thesis
Access StatusOnly available to University of Melbourne staff and students, login required
© 2014 Dr. Jennifer Sun-Fah Jackson
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.
Keywordsdepression; adolescence; inflammation; brain development; family
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