ArticleBrain, behavior, & immunity - health2024
Neural and immune interactions linking early life stress and anhedonia.
Article in Brain, behavior, & immunity - health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- A unified theory of restrictive and addictive eating: a life course model integrating generational transmission, neurodevelopmental risk, and ultra-processed food use disorder-a theoretical review.Journal of eating disorders · 2026Review
- Peptide signaling in the paraventricular thalamus contributes to disrupted adult reward behaviors after early-life adversity.bioRxiv : the preprint server for biology · 2026Article
- Characterization of inflammatory and neurofunctional markers in the context of early life stress among a clinical sample of people maintained on buprenorphine for opioid use disorder.Brain, behavior, & immunity - health · 2025Article
Corrections and comments
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Authors and funding
1 author.
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No grant is acknowledged in the PubMed record.
Abstract
Early experiences of stress and adversity are associated with blunted reward sensitivity and altered reward learning. Meanwhile, anhedonia is characterized by impairments in reward processing, including motivation, effort, and pleasure. Early life stress (ELS) and anhedonia share psychological, behavioral, and neurobiological correlates, and the system-level interactions that give rise to anhedonia have yet to be fully appreciated. The proposed framework uses a multilevel, multisystem approach to aid in understanding neural-immune interactions that link ELS and anhedonia. The interactions linking anhedonia and ELS presented here include reduced reward sensitivity, alterations in hypothalamic-pituitary-adrenal (HPA) axis response, elevated inflammatory cytokines or physiological markers of stress, and blunted reward circuitry functioning along the mesocorticolimbic pathway. The clinical implications and areas for future research are also discussed. Ultimately, this research may inform the development of more specific and individualized treatments for anhedonia.
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Registered trials
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