Neurobiological mechanisms of anhedonia in adolescents with mood disorders: A scoping review

BACKGROUND: Anhedonia-a core symptom of mood disorders-reflects impairments in both reward anticipation and reward consumption. While its neurobiological underpinnings have been extensively studied in adults, considerably less is known about adolescent populations, despite critical neurodevelopmental changes during this period. This scoping review aims to map current evidence onto neurobiological correlates of anhedonia in adolescents with mood disorders. METHODS: A systematic search was conducted in PubMed and PsycInfo to identify studies investigating anhedonia in adolescents with mood disorders using neuroimaging techniques. Due to heterogeneity in study design and outcomes, findings were synthesized narratively. RESULTS: Twenty-one articles met the inclusion criteria, reporting on 1278 patients. The analysis revealed that anhedonia involves (1) increased frontal and decreased striatal activity during reward/incentive processing, and activation of regions of the limbic system during loss-related error processing; (2) striatal and corticolimbic activity during emotional processing; (3) reduced medial prefrontal cortex activity during cognitive processing; (4) involvement of corticostriatal and corticolimbic functional connectivity networks; (5) an inverse association between cerebral blood flow in corticolimbic and frontal regions in cerebral blood flow analysis; (6) altered alpha and theta activity and reduced cortical reactivity, and that; (7) GABA involvement in anhedonia remains inconclusive. CONCLUSIONS: The neurobiological signatures of anhedonia in adolescents appear to involve altered activation and connectivity in reward-related circuits, particularly during anticipatory and error-processing phases. These findings underscore the need for greater methodological consistency, standardized phenotyping of anhedonia, and longitudinal studies to better understand developmental trajectories and inform early interventions.