Anhedonia in Depression and Schizophrenia: Brain Reward and Aversion Circuits

Anhedonia, which is defined as markedly diminished interest or pleasure, is a prominent symptom of psychiatric disorders, most notably major depressive disorder (MDD) and schizophrenia. Anhedonia is considered a transdiagnostic symptom that is associated with deficits in neural reward and aversion functions. Here, we review the characteristics of anhedonia in depression and schizophrenia as well as shared or disorder-specific anhedonia-related alterations in reward and aversion pathways of the brain. In particular, we highlight that anhedonia is characterized by impairments in anticipatory pleasure and integration of reward-related information in MDD, whereas anhedonia in schizophrenia is associated with neurocognitive deficits in representing the value of rewards. Dysregulation of the frontostriatal circuit and mesocortical and mesolimbic circuit systems may be the transdiagnostic neurobiological basis of reward and aversion impairments underlying anhedonia in these two disorders. Blunted aversion processing in depression and relatively strong aversion in schizophrenia are primarily attributed to the dysfunction of the habenula, insula, amygdala, and anterior cingulate cortex. Furthermore, patients with schizophrenia appear to exhibit greater abnormal activation and extended functional coupling than those with depression. From a transdiagnostic perspective, understanding the neural mechanisms underlying anhedonia in patients with psychiatric disorders may help in the development of more targeted and efficacious treatment and intervention strategies.

Automated summary

Anhedonia, a prominent symptom in psychiatric disorders such as major depressive disorder (MDD) and schizophrenia, is associated with deficits in neural reward and aversion functions. In MDD, anhedonia is characterized by impairments in anticipatory pleasure and integration of reward-related information, while in schizophrenia it is associated with neurocognitive deficits in representing the value of rewards. Dysregulation of frontostriatal, mesocortical, and mesolimbic circuits may underlie reward and aversion impairments in anhedonia. Dysfunction of the habenula, insula, amygdala, and anterior cingulate cortex contribute to blunted aversion processing in depression and relatively strong aversion in schizophrenia. Patients with schizophrenia show greater abnormal activation and extended functional coupling compared to those with depression. Understanding the neural mechanisms underlying anhedonia in psychiatric disorders can aid in developing targeted and efficacious treatment strategies.