Abstract
Many neuroimaging studies have investigated reward processing dysfunction in major depressive disorder. These studies have led to the common idea that major depressive disorder is associated with blunted responses within the reward circuit, particularly in the ventral striatum. Yet, the link between major depressive disorder and reward-related responses in other regions remains inconclusive, thus limiting our understanding of the pathophysiology of major depressive disorder. To address this issue, we performed a coordinate-based meta-analysis of 41 whole-brain neuroimaging studies encompassing reward-related responses from a total of 794 patients with major depressive disorder and 803 healthy controls. Our findings argue against the common idea that major depressive disorder is primarily linked to deficits within the reward system. Instead, our results demonstrate that major depressive disorder is associated with opposing abnormalities in the reward circuit: hypo-responses in the ventral striatum and hyper-responses in the orbitofrontal cortex. The current findings suggest that dysregulated corticostriatal connectivity may underlie reward-processing abnormalities in major depressive disorder, providing an empirical foundation for a more refined understanding of abnormalities in the reward circuitry in major depressive disorder.
Highlights
Depression is a prevalent mental disorder ranked as the leading non-fatal cause of disability by the World Health Organization[1]
The results indicated that these studies reliably reported greater activation in the left sublenticular extended amygdala in MDD (Table 2; Fig. 2 Opposing abnormalities in the reward circuit in response to reward in major depressive disorder. a To examine regions that consistently showed blunted response to reward, 22 studies reporting less activity in response to reward in people with major depressive disorder (MDD) than healthy controls (HC) were synthesized
A growing number of researchers have used neuroimaging methods to enhance our understanding of the underlying pathophysiology of MDD68–70
Summary
Depression is a prevalent mental disorder ranked as the leading non-fatal cause of disability by the World Health Organization[1]. The striatum, which can be divided into dorsal and ventral sections, is the primary input zone for basal ganglia[16,17]. It receives afferent projections from the midbrain, amygdala, and prefrontal cortex (PFC), such as the orbitofrontal cortex (OFC), dorsolateral prefrontal cortex (dlPFC), ventromedial prefrontal cortex (vmPFC), and anterior cingulate cortex (ACC)[16,17]. The striatum has been proposed to play an important role in the onset and course of MDD, with longitudinal studies demonstrating that blunted activation in the VS during reward anticipation predicts the emergence of depressive symptoms and disorder[30,31] and deepbrain stimulation studies using it as a treatment target for treatment-resistant depression[32]
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