Dataset Information

Understanding the neurobiological basis of anhedonia in major depressive disorder - evidence for reduced neural activation during reward and loss processing.

ABSTRACT:

Background

Anhedonia is a key symptom of major depressive disorder (MDD). Anhedonia is associated with aberrant reward processing, but whether it might interfere similarly with the neural processing of aversive stimuli, such as monetary loss, remains unknown. We aimed to investigate potential associations between anhedonia and neural response during reward and loss processing in patients with MDD.

Methods

We investigated blood-oxygen-level-dependent response in the orbitofrontal cortex, cingulate cortex, insula and basal ganglia during monetary reward and loss processing in 182 patients with MDD, using a card-guessing paradigm. We measured anhedonia with the Social and Physical Anhedonia Scale (SASPAS), and we tested for the main and interaction effects of SASPAS scores and the experimental condition (reward or loss) in a full factorial model.

Results

We detected a negative main effect of anhedonia, as well as a significant interaction effect of anhedonia and the experimental condition, on orbitofrontal and insular neural response. Post hoc analyses revealed that the interaction was driven by a significant association between higher anhedonia scores and hypoactivation during loss processing. We observed no significant association between anhedonia and neural response during reward processing.

Limitations

This study had a cross-sectional design.

Conclusion

Our findings confirmed that altered neural processing in the orbitofrontal cortex and insula is a neurobiological feature of anhedonic symptomatology in people with MDD. The pronounced association between anhedonia and blunted neural response during loss processing supports a broader concept for the neurobiological basis of anhedonia. Hence, MDD with anhedonic features might be characterized by reduced neural response to external stimuli, potentially because of amotivation.

SUBMITTER: Steinmann LA

PROVIDER: S-EPMC9377543 | biostudies-literature | 2022 Jul-Aug

REPOSITORIES: biostudies-literature

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Publications

Understanding the neurobiological basis of anhedonia in major depressive disorder - evidence for reduced neural activation during reward and loss processing.

Steinmann Lavinia A LA Dohm Katharina K Goltermann Janik J Richter Maike M Enneking Verena V Lippitz Marcia M Repple Jonathan J Mauritz Marco M Dannlowski Udo U Opel Nils N

Journal of psychiatry & neuroscience : JPN 20220701 4

<h4>Background</h4>Anhedonia is a key symptom of major depressive disorder (MDD). Anhedonia is associated with aberrant reward processing, but whether it might interfere similarly with the neural processing of aversive stimuli, such as monetary loss, remains unknown. We aimed to investigate potential associations between anhedonia and neural response during reward and loss processing in patients with MDD.<h4>Methods</h4>We investigated blood-oxygen-level-dependent response in the orbitofrontal c ...[more]

PMID: 35948341

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Project description:An inhibited neural response to reward is typical of clinical depression and can predict an individual's overall depressive symptoms. However, the mechanism underlying this are unclear. Previous studies have found that anhedonia and inattention may mediate the relationship between reward sensitivity and depressive symptoms. Therefore, this study aimed to verify the relationship between reward sensitivity and overall depressive symptoms in a depressive tendency sample as well as to explore the mechanism underlying the ability of neural responses to reward to predict overall depressive symptoms via a mediation model. Sixty-four participants (33 with depressive tendencies and 31 without; dichotomized by BDI-II) finished simple gambling tasks while their event-related potential components (ERPs) were recorded and compared. Linear regression was conducted to verify the predictive effect of ERPs on overall depressive symptoms. A multiple mediator model was used, with anhedonia and distractibility as mediators reward sensitivity and overall depressive symptoms. The amplitude of reward positivity (ΔRewP) was greater in healthy controls compared to those with depressive tendencies (p = 0.006). Both the gain-locked ERP component (b = - 1.183, p = 0.007) and the ΔRewP (b = - 0.991, p = 0.024) could significantly negatively predict overall depressive symptoms even after controlling for all anxiety symptoms. The indirect effects of anhedonia and distractibility were significant (both confidence intervals did not contain 0) while the direct effect of reward sensitivity on depressive symptom was not significant (lower confidence interval = - 0.320, upper confidence interval = 0.065). Individuals with depressive tendencies display impaired neural responses to reward compared to healthy controls and reduced individual neural responses to reward may reflect the different biotypes of depression such as anhedonia and inattention.

Project description:Background: Behavioral tasks focusing on different subdomains of reward processing may provide more objective and quantifiable measures of anhedonia and impaired motivation compared with clinical scales. Typically, single tasks are used in relatively small studies to compare cases and controls in one indication, but they are rarely included in larger multisite trials. This is due to limited systematic standardization as well as the challenges of deployment in international studies and stringent adherence to the high regulatory requirements for data integrity. The Reward Task Optimization Consortium (RTOC) was formed to facilitate operational implementation of reward processing tasks, making them suitable for use in future large-scale, international, multisite drug development studies across multiple indications. The RTOC clinical study aims to conduct initial optimization of a set of tasks in patients with major depressive disorder (MDD) or schizophrenia (SZ). Methods: We will conduct a multicenter study across four EU countries. Participants (MDD = 37, SZ = 37, with ≤80 age- and gender-matched healthy volunteers) will attend a study visit comprising screening, self-report and clinically rated assessments of anhedonia and symptom severity, and three reward processing tasks; specifically, the Grip Strength Effort task, the Doors task, and the Reinforcement Learning Working Memory task. The Grip Strength Effort and Doors tasks include simultaneous electroencephalography/event-related potential recordings. Outcomes will be compared using a two-way group design of MDD and SZ with matched controls, respectively. Further analyses will include anhedonia assessment scores as covariates. Planned analyses will assess whether our findings replicate previously published data, and multisite deployment will be evaluated through assessments of quality and conduct. A subset of participants will complete a second visit, to assess test-retest reliability of the task battery. Discussion: This study will evaluate the operational deployment of three reward processing tasks to the regulatory standards required for use in drug development trials. We will explore the potential of these tasks to differentiate patients from controls and to provide a quantitative marker of anhedonia and/or impaired motivation, establishing their usefulness as endpoints in multisite clinical trials. This study should demonstrate where multifaceted reward deficits are similar or divergent across patient populations. Registration: ClinicalTrials.gov (NCT04024371).

Dataset Information

Understanding the neurobiological basis of anhedonia in major depressive disorder - evidence for reduced neural activation during reward and loss processing.

Background

Methods

Results

Limitations

Conclusion

Publications

Understanding the neurobiological basis of anhedonia in major depressive disorder - evidence for reduced neural activation during reward and loss processing.

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