Investigating neural responses to reward and childhood stress exposure in relation to depressive symptoms

Background: Early life stress is a robust predictor of adult depression, yet the mechanisms underlying this relationship remain unclear. Evidence shows early life stress impacts brain circuits involved in reward processing, linked to depression. However, although the link between early life stress and blunted neural responses to rewards appears to be associated with depressive symptoms, meta-analyses reveal significant heterogeneity in effect sizes. Aim of the study: The objective of the present cross-sectional study was to assess the relationship between early life stress and depressive symptoms, specifically examining whether a neural marker of reward processing, Reward Positivity (RewP), moderates this relationship in a large sample of emerging adults. Materials and methods: A cross-sectional investigation was conducted, utilizing a large dataset of emerging adults (N = 820) from the Coscience EEG project. Childhood stress was retrospectively assessed using the Childhood Trauma Questionnaire (CTQ). General depressive symptoms were assessed using the Beck Depression Inventory-II (BDI-II). Participants performed a monetary gambling task to elicit neural responses to rewards and losses. RewP was quantified as the mean amplitude (200-300 ms) at frontocentral electrodes. Linear regression models were employed to test the interaction between CTQ scores and RewP in predicting depressive symptoms. Results: Greater exposure to early life stress was significantly associated with higher levels of depressive symptoms, confirming the well-established link between childhood adversity and adult depression. However, contrary to the moderation hypothesis, the RewP did not moderate this association at either electrode analyzed. Conclusion: The present findings confirm that early life stress is robustly associated with depressive symptomatology in emerging adulthood, but do not support the hypothesis that the reward processing moderates this link in a community sample of this age range. The convergent null findings across both electrode sites suggest that the previously documented buffering role of the RewP may be specific to adolescence, type of task used, or confined to clinical and higher-adversity populations. Future research employing social reward paradigms, longitudinal designs, and recruitment from trauma-exposed samples may provide clarity on the conditions under which the RewP operates as a neural moderator of risk for depression. Keywords: Anhedonia, Childhood stress, ERPs, Reward, Depression