ArticleBrain, behavior, and immunity2024
Major stress in early childhood strengthens the association between peripheral inflammatory activity and corticostriatal responsivity to reward.
Article in Brain, behavior, and immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Inflammatory cytokine alterations in genetic and clinical high risk groups of psychosis: a systematic review and network meta-analysis.Psychological medicine · 2026Pooled it
- Observational
- Stage-specific effects of early-life tobacco exposure on mental health, inflammation, and brain structure-function coupling.Translational psychiatry · 2026Article
- Neural response to reward as a potential pathway from inflammation to anhedonia in adolescents at risk for depression.Brain, behavior, & immunity - health · 2026Article
- Reward-related activation of fronto-striatal regions scaled negatively with C-reactive protein.Psychological medicine · 2025Article
- An Integrated Immuno-Reward Model of Adolescent Depression: Theory, Evidence, and Implications.Current directions in psychological science · 2025Article
- Childhood exposure to danger increases Black youths' alcohol consumption, accelerated aging, and cardiac risk as young adults: A test of the incubation hypothesis.Development and psychopathology · 2025Article
- A dyadic longitudinal analysis of parent-adolescent inflammation trends and the role of shared socioeconomic characteristics on family inflammation.Brain, behavior, & immunity - health · 2024Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundSevere, chronic stress during childhood accentuates vulnerability to mental and physical health problems across the lifespan. To explain this phenomenon, the neuroimmune network hypothesis proposes that childhood stressors amplify signaling between peripheral inflammatory cells and developing brain circuits that support processing of rewards and threats. Here, we conducted a preliminary test of the basic premises of this hypothesis.
methods180 adolescents (mean age = 19.1 years; 68.9 % female) with diverse racial and ethnic identities (56.1 % White; 28.3 % Hispanic; 26.1 % Asian) participated. The Childhood Trauma Interview was administered to quantify early adversity. Five inflammatory biomarkers were assayed in antecubital blood - C-reactive protein, tumor necrosis factor-a, and interleukins-6, -8, and -10 - and were averaged to form a composite score. Participants also completed a functional MRI task to measure corticostriatal responsivity to the anticipation and acquisition of monetary rewards.
resultsStress exposure and corticostriatal responsivity interacted statistically to predict the inflammation composite. Among participants who experienced major stressors in the first decade of life, higher inflammatory activity covaried with lower corticostriatal responsivity during acquisition of monetary rewards. This relationship was specific to participants who experienced major stress in early childhood, implying a sensitive period for exposure, and were evident in both the orbitofrontal cortex and the ventral striatum, suggesting the broad involvement of corticostriatal regions. The findings were independent of participants' age, sex, racial and ethnic identity, family income, and depressive symptoms.
conclusionsCollectively, the results are consistent with hypotheses suggesting that major stress in childhood alters brain-immune signaling.
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