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Peripheral Inflammation and Activity within Corticostriatal Reward Circuitry: Interactive Roles in Components of Anhedonia during Adolescence
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Thesis/Dissertation
Date
2025-08
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Psychology
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https://doi.org/10.34944/r0yd-9b23
Abstract
Depression is a significant global health burden, affecting millions of people worldwide and contributing to a high level of disability. Despite the availability of treatments, a substantial proportion of individuals experience insufficient treatment response. Anhedonia often is observed in treatment-resistant depression and severe presentations of depression, suggesting that mechanisms underlying anhedonia may be important treatment targets. However, anhedonia is among the most challenging psychiatric symptoms to treat, and the mechanisms underlying this symptom are unclear. This work aimed to deepen our understanding of the neurobiological mechanisms underlying anhedonia, with a specific focus on peripheral inflammation, corticostriatal reward circuitry, and their interaction, in adolescence. Adolescence is a developmental period marked by significant maturation in both reward-related brain function and immune system activity, rendering it a sensitive window for environmental input and the emergence of depression and anhedonia.
This study suggested that there were nuanced associations of inflammatory proteins and reward-related brain function, independently and interactively, with anhedonia in adolescents. Specifically, distinct components of anhedonia (i.e., diminished anticipatory and consummatory pleasure, temporal discounting of reward value, and reward sensitivity) were differentially associated with the interplay between inflammation and reward-related corticostriatal activity. The results also indicated that the interaction between higher levels of inflammatory proteins and distinct reward-related corticostriatal activity were associated with higher levels of anhedonia in the absence of a depression diagnosis. Thus, inflammation-reward pathways could be a mechanism underlying anhedonia across various psychiatric disorders characterized by reward deficits.
Given that current treatments do not effectively target reward-related corticostriatal and inflammatory pathways, this work has potential clinical implications, with a call for a re-evaluation of how anhedonia should be conceptualized and measured across research and clinical settings. Specifically, it is important to parse anhedonia rather than assuming it is a unitary construct, and to standardize the definitions and measurements of anhedonia. Ultimately, the work presented here contributes to a growing body of literature suggesting that inflammation-reward pathways represent promising new targets for the treatment of anhedonia in both depression and other psychiatric disorders.
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