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Animal models of depression show that acute stress negatively impacts functioning in neural regions sensitive to reward and punishment, often manifesting as anhedonic behaviors. However, few human studies have probed stress-induced neural activation changes in relation to anhedonia, which is critical for clarifying risk for affective disorders. Participants (N = 85, 12-14 years-old, 53 female), oversampled for risk of depression, were administered clinical assessments and completed an fMRI guessing task during a baseline (no-stress) period to probe neural response to receipt of rewards and losses. After the initial task run of the fMRI guessing task, participants received an acute stressor and then, were re-administered the guessing task. Including baseline, participants provided up to 10 self-report assessments of life stress and symptoms over a 2 year period. Linear mixed-effects models estimated whether change in neural activation (post- vs. pre-acute stressor) moderated the longitudinal associations between life stress and symptoms. Primary analyses indicated that adolescents with stress-related reductions in right ventral striatum response to rewards exhibited stronger longitudinal associations between life stress and anhedonia severity (β = -0.06, 95%CI[-0.11, -0.02], p = 0.008, p FDR  = 0.048). Secondary analyses showed that longitudinal positive associations between life stress and depression severity were moderated by stress-related increases in dorsal striatum response to rewards (left caudate β = 0.11, 95%CI[0.07,0.17], p < 0.001, p FDR  = 0.002; right caudate β = 0.07, 95%CI[0.02,0.12], p = 0.002, p FDR  = 0.003; left putamen β = 0.09, 95%CI[0.04, 0.14], p < 0.001, p FDR  = 0.002; right putamen β = 0.08, 95%CI[0.03, 0.12], p < 0.001, p FDR  = 0.002). Additionally, longitudinal positive associations among life stress and anxiety severity were moderated by stress-related reductions in dorsal anterior cingulate cortex (β = -0.07, 95%CI[-0.12,.02], p = 0.008, p FDR  = 0.012) and right anterior insula (β = -0.07, 95%CI[-0.12,-0.02], p = 0.002, p FDR  = 0.006) response to loss. All results held when adjusting for comorbid symptoms. Results show convergence with animal models, highlighting mechanisms that may facilitate stress-induced anhedonia as well as a separable pathway for the emergence of depressive and anxiety symptoms., (© 2024. The Author(s).)

Suicide is a leading cause of death, and presently, there is no definitive clinical indicator of future suicide behaviors. Anhedonia, a transdiagnostic symptom reflecting diminished ability to experience pleasure, has recently emerged as a risk factor for suicidal thoughts and behaviors (STBs). This overview, therefore, has the following aims. First, prior research relating anhedonia to STBs will be reviewed, with a particular focus on clarifying whether anhedonia is more closely associated with suicidal thoughts versus behaviors. Second, the National Institute of Mental Health's Research Domain Criteria Positive Valence Systems provide a useful heuristic to probe anhedonia across different units of analysis, including clinical symptoms, behaviors, neural mechanisms, and molecular targets. Accordingly, anhedonia-related constructs linked to STBs will be detailed as well as promising next steps for future research. Third, although anhedonia is not directly addressed in leading suicide theories, this review will provide potential inroads to explore anhedonia within diathesis-stress and interpersonal suicide frameworks. Last, novel approaches to treat anhedonia as a means of reducing STBs will be examined., (© 2022. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Anhedonia is a transdiagnostic risk factor implicated in mental illness onset, treatment non-response, and suicidal behaviors. Prior cross-sectional research in adults has shown that anhedonia is associated with reduced dorsal striatal volume, but it is unknown whether this relationship extends to adolescents and whether reduced striatal volume prospectively predicts anhedonia. To address these gaps, the current study investigated whether striatal volume predicted anhedonia severity in adolescents. At baseline, healthy female adolescents aged 12-14 years (n=50) completed a clinical assessment, and structural MRI data were acquired on a 3 Tesla MR scanner. While in the scanner, participants also completed a peer feedback task where subjective ratings following peer 'acceptance' or 'rejection' were obtained. At the three-month follow-up, participants provided self-report assessments of anhedonia, depression, and anxiety symptoms. Three main findings emerged. First, in cross-sectional analyses, right nucleus accumbens volume was inversely related to anhedonia severity. Second, reduced bilateral putamen volume prospectively predicted anhedonia severity while controlling for baseline anhedonia, depression, and anxiety symptoms. Third, a blunted subjective response to peer acceptance (ie, neutral response to positive feedback), but not a more negative subjective response to peer rejection, contributed to anhedonia severity, but only among youth with smaller putamen volume. Collectively, these results suggest that smaller volume in striatal regions critically implicated in reward processing is associated with current and future anhedonic symptoms among healthy female youth. These anatomical features may confer vulnerability to anhedonia and thus, may inform early identification of individuals at high risk for mental illness.

Anhedonia is a prominent symptom in neuropsychiatric disorders, most markedly in major depressive disorder (MDD) and schizophrenia (SZ). Emerging evidence indicates an overlap in the neural substrates of anhedonia between MDD and SZ, which supported a transdiagnostic approach. Therefore, we used activation likelihood estimation (ALE) meta-analysis of functional magnetic resonance imaging studies in MDD and SZ to examine the neural bases of three subdomains of anhedonia: consummatory anhedonia, anticipatory anhedonia and emotional processing. ALE analysis focused specifically on MDD or SZ was used later to dissociate specific anhedonia-related neurobiological impairments from potential disease general impairments. ALE results revealed that consummatory anhedonia was associated with decreased activation in ventral basal ganglia areas, while anticipatory anhedonia was associated with more substrates in frontal-striatal networks except the ventral striatum, which included the dorsal anterior cingulate, middle frontal gyrus and medial frontal gyrus. MDD and SZ patients showed similar neurobiological impairments in anticipatory and consummatory anhedonia, but differences in the emotional experience task, which may also involve affective/mood general processing. These results support that anhedonia is characterized by alterations in reward processing and relies on frontal-striatal brain circuitry. The transdiagnostic approach is a promising way to reveal the overall neurobiological framework that contributes to anhedonia and could help to improve targeted treatment strategies., Competing Interests: Conflict of interest Dr. Öngür has served on a Scientific Advisory Board for Lilly Inc. in 2013. Author Bei Zhang, Author Pan Lin, Author Huqing Shi, Author Randy P Auerbach, Author Xiaosheng Wang, Author Shuqiao Yao and Author Xiang Wang declare that they have no conflict of interest.

Objective: Although depression and anxiety often have distinct etiologies, they frequently co-occur in adolescence. Recent initiatives have underscored the importance of developing new ways of classifying mental illness based on underlying neural dimensions that cut across traditional diagnostic boundaries. Accordingly, the aim of the study was to clarify reward-related neural circuitry that may characterize depressed-anxious youth.Method: The Boston Adolescent Neuroimaging of Depression and Anxiety Human Connectome Project tested group differences regarding subcortical volume and nucleus accumbens activation during an incentive processing task among 14- to 17-year-old adolescents presenting with a primary depressive and/or anxiety disorder (n = 129) or no lifetime history of mental disorders (n = 64). In addition, multimodal modeling examined predictors of depression and anxiety symptom change over a 6-month follow-up period.Results: Our findings highlighted considerable convergence. Relative to healthy youth, depressed-anxious adolescents exhibited reduced nucleus accumbens volume and activation following reward receipt. These findings remained when removing all medicated participants (∼59% of depressed-anxious youth). Subgroup analyses comparing anxious-only, depressed-anxious, and healthy youth also were largely consistent. Multimodal modeling showed that only structural alterations predicted depressive symptoms over time.Conclusion: Multimodal findings highlight alterations within nucleus accumbens structure and function that characterize depressed-anxious adolescents. In the current hypothesis-driven analyses, however, only reduced nucleus accumbens volume predicted depressive symptoms over time. An important next step will be to clarify why structural alterations have an impact on reward-related processes and associated symptoms. [ABSTRACT FROM AUTHOR]

Background: Numerous theories have posited that stressors occurring over the lifespan may exert a cumulative effect on psychological and biological processes that increase individuals' risk for a variety of mental and physical health problems. Given the difficulty associated with assessing lifetime stress exposure, however, few empirical studies have directly tested these cumulative risk models of psychopathology and human health. Method: To address this issue, we examined the usability, acceptability, concurrent validity, and predictive validity of the recently developed Stress and Adversity Inventory for Adolescents (Adolescent STRAIN) in 338 youth (Mage = 15.64; 229 females) seeking mental health treatment. Results: The Adolescent STRAIN achieved high acceptability and was completed in approximately 25 min (interquartile range: 20–32 min). Concurrent associations with other measures of early adversity (Childhood Trauma Questionnaire‐Short Form) and interpersonal stress (Revised Peer Experiences Questionnaire) were very good (rs = .50–.59). In analyses that adjusted for participants' age, sex, and race, the STRAIN was significantly associated with depression, anxiety, and anhedonia severity; general mental and physical health complaints; risky behavior engagement; and number of interviewer‐based psychiatric diagnoses (βs = .16–.52; risk ratios = 1.006–1.014). Contrary to classic theories of stress which assume that different stressors exert similar effects on health, substantial differences were observed across the two stressor types, twelve life domains, and five core social‐psychological characteristics assessed by the Adolescent STRAIN. Conclusions: These data confirm the relevance of lifetime stress exposure for multiple health outcomes in adolescence, which can in turn inform existing theories of lifespan health. Because stress is a common presenting problem in hospitals and clinics, these data also suggest the possibility of using the Adolescent STRAIN to generate stress exposure profiles for case conceptualization and treatment planning purposes. [ABSTRACT FROM AUTHOR]

The article focuses on the reasons behind treatment failure of anhedonia, which is reduced ability to experiencing pleasure resulting in suicidal behaviors. It discusses the National Institute of Mental Health's Research Domain Criteria initiative having framework for functioning like Positive Valence Systems.

Background Adolescent depression and suicide are pressing public health concerns, and identifying key differences among suicide ideators and attempters is critical. The goal of the current study is to test whether depressed adolescent suicide attempters report greater anhedonia severity and exhibit aberrant effort–cost computations in the face of uncertainty. Methods Depressed adolescents ( n =101) ages 13–19 years were administered structured clinical interviews to assess current mental health disorders and a history of suicidality (suicide ideators=55, suicide attempters=46). Then, participants completed self-report instruments assessing symptoms of suicidal ideation, depression, anhedonia, and anxiety as well as a computerized effort–cost computation task. Results Compared with depressed adolescent suicide ideators, attempters report greater anhedonia severity, even after concurrently controlling for symptoms of suicidal ideation, depression, and anxiety. Additionally, when completing the effort–cost computation task, suicide attempters are less likely to pursue the difficult, high value option when outcomes are uncertain. Follow-up, trial-level analyses of effort–cost computations suggest that receipt of reward does not influence future decision-making among suicide attempters, however, suicide ideators exhibit a win–stay approach when receiving rewards on previous trials. Limitations Findings should be considered in light of limitations including a modest sample size, which limits generalizability, and the cross-sectional design. Conclusions Depressed adolescent suicide attempters are characterized by greater anhedonia severity, which may impair the ability to integrate previous rewarding experiences to inform future decisions. Taken together, this may generate a feeling of powerlessness that contributes to increased suicidality and a needless loss of life. [ABSTRACT FROM AUTHOR]

Anhedonia is a prominent symptom in neuropsychiatric disorders, most markedly in major depressive disorder (MDD) and schizophrenia (SZ). Emerging evidence indicates an overlap in the neural substrates of anhedonia between MDD and SZ, which supported a transdiagnostic approach. Therefore, we used activation likelihood estimation (ALE) meta-analysis of functional magnetic resonance imaging studies in MDD and SZ to examine the neural bases of three subdomains of anhedonia: consummatory anhedonia, anticipatory anhedonia and emotional processing. ALE analysis focused specifically on MDD or SZ was used later to dissociate specific anhedonia-related neurobiological impairments from potential disease general impairments. ALE results revealed that consummatory anhedonia was associated with decreased activation in ventral basal ganglia areas, while anticipatory anhedonia was associated with more substrates in frontal-striatal networks except the ventral striatum, which included the dorsal anterior cingulate, middle frontal gyrus and medial frontal gyrus. MDD and SZ patients showed similar neurobiological impairments in anticipatory and consummatory anhedonia, but differences in the emotional experience task, which may also involve affective/mood general processing. These results support that anhedonia is characterized by alterations in reward processing and relies on frontal-striatal brain circuitry. The transdiagnostic approach is a promising way to reveal the overall neurobiological framework that contributes to anhedonia and could help to improve targeted treatment strategies. Electronic supplementary material The online version of this article (doi:10.1007/s11682-015-9457-6) contains supplementary material, which is available to authorized users.

For several decades, resting electroencephalogram (EEG) alpha oscillations have been used to characterize neurophysiological alterations related to major depressive disorder. Prior research has generally focused on frontal alpha power and asymmetry despite resting alpha being maximal over posterior electrode sites. Research in depressed adults has shown evidence of hemispheric asymmetry for posterior alpha power, however, the resting posterior alpha-depression link among adolescents remains unclear. To clarify the role of posterior alpha among depressed adolescents, the current study acquired eyes-closed 128-channel resting EEG data from 13 to 18 year-old depressed (n = 31) and healthy (n = 35) female adolescents. Results indicated a significant group by hemisphere interaction, as depressed adolescents exhibited significantly larger posterior alpha (i.e., lower brain activity) over the right versus left hemisphere, whereas healthy adolescents showed no hemispheric differences. Relatively greater alpha over the right versus left hemisphere correlated with depression symptoms, anhedonia symptoms, rumination, and self-criticism. Further, depressed adolescents had reduced overall posterior alpha compared to healthy youth; though, no associations with symptoms and related traits emerged. Resting posterior alpha may be a promising neurophysiological index of adolescent depression, and more broadly, may relate to risk factors characterized by enhanced perseveration. • Depressed youth are characterized by increased resting posterior alpha asymmetry. • Depressed youth exhibit reduced overall posterior alpha compared to healthy youth. • Posterior alpha asymmetry correlates with depression-related symptoms and traits. [ABSTRACT FROM AUTHOR]

Identifying risk markers for major depressive disorder (MDD) that persist into remission is key to address MDD's high rate of recurrence. Central to MDD recurrence are the disorder's negative information processing biases, such as heightened responses to errors, which may subsequently impair abilities to monitor performance and adjust behaviors based on environmental demands. However, little is known regarding the neurophysiological correlates of post- error adaptation in depression. The current study investigated event-related potentials (ERPs) and behavioral performance following errors from a flanker task in 58 participants with remitted MDD (rMDD) and 118 healthy controls (HC). Specifically, using trial-level data, we tested: (a) the impact of errors on response-locked ERPs of the current and post-error trials (error-related negativity [ERN] and correct response negativity [CRN]) and (b) longer-term adaptation to errors (ERN/CRN) over the course of the task. Compared to HC, rMDD participants showed a larger ERN to the current trial and smaller habituation in ERN over time. On trials immediately following errors, rMDD participants showed slower reaction times that were predicted by the previous-trial ERN amplitude but comparable accuracy to HC, suggesting a deficient ability to disengage from errors and/or a compensatory effort to mitigate accuracy decrements. Critically, this pattern of responding: (a) was concurrently associated with greater levels of anhedonia symptoms, more severe MDD history, and interpersonal impairment (but lower impairment in life activities) and (b) predicted more anhedonia symptoms at one-year follow-up. Collectively, a hyperactive performance monitoring system may be a useful risk marker for future MDD recurrence. • Used trial-level ERP to test adaptations to errors in remitted depression (rMDD). • rMDD showed enhanced ERN and diminished habituation in ERN over time. • Heightened error responsivity was associated with interpersonal impairment. • Heightened error responsivity predicted increases in anhedonia one year later. [ABSTRACT FROM AUTHOR]