Anhedonia, the reduced ability to experience pleasure, has been critically implicated in a wide range of adolescent mental disorders and suicidal behaviors.1,2 Presently, medication as well as most first-line psychotherapeutic… Click to show full abstract
Anhedonia, the reduced ability to experience pleasure, has been critically implicated in a wide range of adolescent mental disorders and suicidal behaviors.1,2 Presently, medication as well as most first-line psychotherapeutic approaches do not sufficiently address motivational and reward-processing deficits that characterize anhedonia, and thus, treatment failure is common. To overcome limitations of a categorical nosologic system and improve treatments for core dysfunction, the National Institute of Mental Health’s Research Domain Criteria initiative provides a framework for research focusing on core domains of functioning, such as the Positive Valence Systems. Through this lens, research has sought to clarify the neural circuity underlying anhedonia and, in doing so, provide a framework to elucidate how and why anhedonia leads to adverse mental health outcomes across the lifespan. Toward addressing this gap, Pornpattananangkul et al3 leveraged data from the Adolescent Brain and Cognitive Development Study to probe neural circuitry associated with anhedonia in children aged 9 to 10 years. The authors used the initial Adolescent Brain and Cognitive Development data release with reliable functional magnetic resonance imaging (MRI) data (n = 2878), which provides sufficient power for subgroup comparisons among children with anhedonia, low mood, anxiety, and attention-deficit/hyperactivity disorder (ADHD). Examining resting-state functional MRI, the authors found that relative to nonanhedonic children, anhedonic youths were characterized by hypoconnectivity among several large-scale networks, including between arousal-related and rewardrelated regions, which was not present in children with low mood, anxiety, or ADHD. Complementary task-evoked functional MRI data also demonstrated that anhedonic youths exhibited hypoactivation during reward anticipation in similar regions and networks; highlighting domain and context specificity, this blunted reward-related activation did not emerge in the low-mood, anxious, or ADHD youths, and anhedonic children showed blunted responses during reward anticipation but not a working memory task. Given the representativeness and sample size, advanced data analytic approach, and Research Domain Criteria–consistent framework, this study adds to a growing literature that has sought to clarify neural abnormalities linked to anhedonia. It also sheds light on key issues to be addressed moving forward.
               
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