Depression is a leading cause of disability worldwide, and early-onset depression is especially pernicious, given associated consequences such as greater risk of recurrence. Identifying predictors of increased risk for depression is an essential public health priority, particularly in adolescence, which represents a critical period of increased risk for depression (Merikangas et al., 2010). Emerging research suggests that neural measures demonstrate greater precision in distinguishing mental illness than behavioral measures (e.g., Gabrieli et al., 2015). Thus, identifying a reliable, clinically relevant, and objective biomarker, which demonstrates high predictive power, has the potential to advance identification of youth at-risk for depression. Deficits in affective reactivity may be implicated in depression risk in children and adolescents (Kujawa & Burkhouse, 2017). Specifically, there is evidence that youth at increased risk for depression (e.g., maternal depression history) exhibit hypoactivation in mesocorticolimbic regions such as the striatum during positive emotion processing (e.g., reward, happy faces) and hyperactivation in the amygdala in response to sad and fearful stimuli (Kujawa & Burkhouse, 2017). Evidence from a small number of longitudinal neuroimaging studies highlights blunted activation in reward-related regions (e.g., striatum) as a predictor of depressive symptoms and diagnosis (Toenders et al., 2019). Yet, across reward and emotion processing tasks, patterns of activation during negative emotion processing are less consistently associated with prospective prediction of depression. Previous studies harnessing neuroimaging methods in youth have resulted in inconsistent findings due to small sample sizes and cross-sectional designs. To elucidate these inconsistencies, we propose to employ data from the Adolescent Brain Cognitive Development (ABCD) study to test relations between neural reactivity during an emotion processing task, depression symptoms, and depression onset in 9- and 10-year-old youth. In doing so, we seek to explore potential depression vulnerability moderators (i.e., familial history of depression, child sex) in these relationships.