Emotion regulation skills develop substantially across adolescence, a period characterized by emotional challenges and developing regulatory neural circuitry. Adolescence is also a risk period for the new onset of anxiety and depressive disorders, psychopathologies which have long been associated with disruptions in regulation of positive and negative emotions. This paper reviews the current understanding of the role of disrupted emotion regulation in adolescent anxiety and depression, describing findings from self-report, behavioral, peripheral psychophysiological, and neural measures. Self-report studies robustly identified associations between emotion dysregulation and adolescent anxiety and depression. Findings from behavioral and psychophysiological studies are mixed, with some suggestion of specific impairments in reappraisal in anxiety. Results from neuroimaging studies broadly implicate altered functioning of amygdala-prefrontal cortical circuitries, although again, findings are mixed regarding specific patterns of altered neural functioning. Future work may benefit from focusing on designs that contrast effects of specific regulatory strategies, and isolate changes in emotional regulation from emotional reactivity. Approaches to improve treatments based on empirical evidence of disrupted emotion regulation in adolescents are also discussed. Future intervention studies might consider training and measurement of specific strategies in adolescents to better understand the role of emotion regulation as a treatment mechanism.

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Emotion regulation skills develop substantially across adolescence, a period characterized by emotional challenges and developing regulatory neural circuitry. Adolescence is also a risk period for the new onset of anxiety and depressive disorders, psychopathologies which have long been associated with disruptions in regulation of positive and negative emotions. This paper reviews the current understanding of the role of disrupted emotion regulation in adolescent anxiety and depression, describing findings from self-report, behavioral, peripheral psychophysiological, and neural measures. Self-report studies robustly identified associations between emotion dysregulation and adolescent anxiety and depression. Findings from behavioral and psychophysiological studies are mixed, with some suggestion of specific impairments in reappraisal in anxiety. Results from neuroimaging studies broadly implicate altered functioning of amygdala-prefrontal cortical circuitries, although again, findings are mixed regarding specific patterns of altered neural functioning. Future work may benefit from focusing on designs that contrast effects of specific regulatory strategies, and isolate changes in emotional regulation from emotional reactivity. Approaches to improve treatments based on empirical evidence of disrupted emotion regulation in adolescents are also discussed. Future intervention studies might consider training and measurement of specific strategies in adolescents to better understand the role of emotion regulation as a treatment mechanism.

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Adolescence is a critical period of neurocognitive development and increased prevalence of mood pathology. In this cross-sectional study, we replicated developmental patterns of neurocognition and tested whether mood symptoms moderated developmental effects. Participants were 419 adolescents ( n = 246 with current mood disorders) who completed reward-learning and executive-functioning tasks and reported on age, puberty, and mood symptoms. Structural equation modeling revealed a quadratic relationship between puberty and reward-learning performance that was moderated by symptom severity: In early puberty, adolescents reporting higher manic symptoms exhibited heightened reward-learning performance (better maximizing of rewards on learning tasks), whereas adolescents reporting elevated anhedonia showed blunted reward-learning performance. Models also showed a linear relationship between age and executive functioning that was moderated by manic symptoms: Adolescents reporting higher mania showed poorer executive functioning at older ages. Findings suggest neurocognitive development is altered in adolescents with mood pathology and suggest directions for longitudinal studies.

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Both unipolar and bipolar depression have been linked with impairments in executive functioning (EF). In particular, mood symptom severity is associated with differences in common EF, a latent measure of general EF abilities. The relationship between mood disorders and EF is particularly salient in adolescence and young adulthood when the ongoing development of EF intersects with a higher risk of mood disorder onset. However, it remains unclear if common EF impairments have associations with specific symptom dimensions of mood pathology such as blunted positive affect, mood instability, or physiological arousal, or if differences in common EF more broadly relate to what is shared across various symptom domains, such as general negative affect or distress. To address this question, bifactor models can be applied to simultaneously examine the shared and unique contributions of particular mood symptom dimensions. However, no studies to our knowledge have examined bifactor models of mood symptoms in relation to measures of common EF. This study examined associations between common EF and general vs. specific symptom dimensions (anhedonia, physiological arousal, and mania) using structural equation modeling in adolescents and young adults with varying severity of mood symptoms (n = 495, ages = 13–25 years, 68.69% female). A General Depression factor capturing shared variance across symptoms statistically predicted lower Common EF. Additionally, a factor specific to physiological arousal was associated with lower Common EF. Anhedonia-specific and Mania-specific factors were not significantly related to Common EF. Altogether, these results indicate that deficits in common EF are driven by, or reflect, general features of mood pathology that are shared across symptom dimensions but are also specifically associated with physiological arousal.