| Summary: | Anhedonia has been suggested as a possible biomarker for depression. Moreover many studies have shown that symptoms of anhedonia are associated with a dysfunction in the neural circuits for reward processing. Given that depression typically begins during adolescence and has high rates of reoccurrence, examining reward function in adolescence could help us understand the aetiology, pathophysiology and the course of depression as well as perhaps even aid the development of new treatments. This thesis is a composition of four studies. The first of these studies examined the neural response to the anticipation, effort and consummation of reward and aversion in adolescents at increased risk for depression. This is the first study that we know of that has examined the neural response to the sub components of reward and aversion; anticipation, effort and consumption in adolescents at risk of depression. We found overall blunted response to both reward and aversion in the at risk group which is what we would have hypothesized given the previous work using a similar task in people both recovered from depression and young people with a family history of depression. The second study extended this work by including a group of adolescents with a clinical diagnosis of depression and collapsing across the groups using a dimensional approach. Dimensional analysis was also then used to examine the relationship between brain activity in regions of interest and depression and anhedonia symptoms. Results of this study revealed decreasing brain responses in key brain regions implicated in the aetiology of depression for the anticipation, effort and consummation of reward and aversion with increasing symptoms of depression and anhedonia. This study extends the previous literature in a number of ways. Firstly, it is the first study examining the neural response to the sub components of reward and aversion processing: anticipation, effort and consummation in depression. Further it is the first study examining how this is related to a range of depression severities in young people. The results of this study finds that there are indeed deficits in key neural regions involved in the processing of reward and punishment and that these deficits are correlated with symptom severity, suggesting possible neural biomarkers for depression. Given that the key resting-state functional connectivity (RSFC) networks have been reported dysfunctional in depression, the remaining two studies of this thesis aimed at investigating the RSFC. Study 3 examined adolescents at risk of depression while study 4 again used a more dimensional approach by combining data of those at risk with adolescents also with a clinical diagnoses of depression. Results of these studies extend current literature in adults by investigating adolescents. Secondly they extend the current knowledge of RSFC in depression by examining the relationship between depression symptoms and RSFC in a dimensional manner. This work shows that young people across a range of depression symptoms show similar patterns of RSFC deficits to previous studies in adults. However this work extends the data also by examining correlations between the RSFC in key networks such as the Cognitive Control Network, the Default Mode Network and the Salience Network and depression symptoms and also anhedonia symptoms. Developing behavioural and pharmacological treatments that target these specific deficits in young individuals might improve the success rate for depression treatment that is currently at a low level of around 40%.
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