Reward-related neural correlates in adolescents with excess body weight.
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ABSTRACT:
SUBMITTER: Bhutani S
PROVIDER: S-EPMC8020479 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IntroductionNeuroscience evidence suggests that adolescent obesity is linked to brain dysfunctions associated with enhanced reward and somatosensory processing and reduced impulse control during food processing. Comparatively less is known about the role of more stable brain structural measures and their link to personality traits and neuropsychological factors on the presentation of adolescent obesity. Here we aimed to investigate regional brain anatomy in adolescents with excess weight vs. lean controls. We also aimed to contrast the associations between brain structure and personality and cognitive measures in both groups.MethodsFifty-two adolescents (16 with normal weight and 36 with excess weight) were scanned using magnetic resonance imaging and completed the Sensitivity to Punishment and Sensitivity to Reward Questionnaire (SPSRQ), the UPPS-P scale, and the Stroop task. Voxel-based morphometry (VBM) was used to assess possible between-group differences in regional gray matter (GM) and to measure the putative differences in the way reward and punishment sensitivity, impulsivity and inhibitory control relate to regional GM volumes, which were analyzed using both region of interest (ROI) and whole brain analyses. The ROIs included areas involved in reward/somatosensory processing (striatum, somatosensory cortices) and motivation/impulse control (hippocampus, prefrontal cortex).ResultsExcess weight adolescents showed increased GM volume in the right hippocampus. Voxel-wise volumes of the second somatosensory cortex (SII) were correlated with reward sensitivity and positive urgency in lean controls, but this association was missed in excess weight adolescents. Moreover, Stroop performance correlated with dorsolateral prefrontal cortex volumes in controls but not in excess weight adolescents.ConclusionAdolescents with excess weight have structural abnormalities in brain regions associated with somatosensory processing and motivation.
| S-EPMC3504042 | biostudies-literature
Project description:Obese adolescents suffer negative social experiences, but no studies have examined whether obesity is associated with dysfunction of the social brain or whether social brain abnormalities relate to disadvantageous traits and social decisions. We aimed at mapping functional activation differences in the brain circuitry of social decision making in adolescents with excess versus normal weight, and at examining whether these separate patterns correlate with reward/punishment sensitivity, disordered eating features, and behavioral decisions. In this fMRI study, 80 adolescents aged 12 to 18 years old were classified in two groups based on age adjusted body mass index (BMI) percentiles: normal weight (n?=?44, BMI percentiles 5th-84th) and excess weight (n?=?36, BMI percentile???85th). Participants were scanned while performing a social decision-making task (ultimatum game) in which they chose to "accept" or "reject" offers to split monetary stakes made by another peer. Offers varied in fairness (Fair vs. Unfair) but in all cases "accepting" meant both players win the money, whereas "rejecting" meant both lose it. We showed that adolescents with excess weight compared to controls display significantly decreased activation of anterior insula, anterior cingulate, and midbrain during decisions about Unfair versus Fair offers. Moreover, excess weight subjects show lower sensitivity to reward and more maturity fears, which correlate with insula activation. Indeed, blunted insula activation accounted for the relationship between maturity fears and acceptance of unfair offers. Excess weight adolescents have diminished activation of brain regions essential for affective tracking of social decision making, which accounts for the association between maturity fears and social decisions.
| S-EPMC6869409 | biostudies-literature
Project description:BackgroundThere has been growing interest under the Research Domain Criteria initiative to investigate behavioral constructs and their underlying neural circuitry. Abnormalities in reward processes are salient across psychiatric conditions and may precede future psychopathology in youth. However, the neural circuitry underlying such deficits has not been well defined. Therefore, in this pilot, we studied youth with diverse psychiatric symptoms and examined the neural underpinnings of reward anticipation, attainment, and positive prediction error (PPE, unexpected reward gain). Clinically, we focused on anhedonia, known to reflect deficits in reward function.MethodsTwenty-two psychotropic medication-free youth, 16 with psychiatric symptoms, exhibiting a full range of anhedonia, were scanned during the Reward Flanker Task. Anhedonia severity was quantified using the Snaith-Hamilton Pleasure Scale. Functional magnetic resonance imaging analyses were false discovery rate corrected for multiple comparisons.ResultsAnticipation activated a broad network, including the medial frontal cortex and ventral striatum, while attainment activated memory and emotion-related regions such as the hippocampus and parahippocampal gyrus, but not the ventral striatum. PPE activated a right-dominant fronto-temporo-parietal network. Anhedonia was only correlated with activation of the right angular gyrus during anticipation and the left precuneus during PPE at an uncorrected threshold.LimitationsFindings are preliminary due to the small sample size.ConclusionsThis pilot characterized the neural circuitry underlying different aspects of reward processing in youth with diverse psychiatric symptoms. These results highlight the complexity of the neural circuitry underlying reward anticipation, attainment, and PPE. Furthermore, this study underscores the importance of RDoC research in youth.
| S-EPMC5453853 | biostudies-literature
Project description:IntroductionIncreased inflammation has been implicated in many psychiatric conditions across ages. We previously reported relationships between blood cytokine levels and anhedonia, the decreased capacity to experience pleasure, as well as with reward brain activation in adolescents with psychiatric symptoms. Here, we sought to extend this work in a larger cohort of adolescents with psychiatric symptoms and assess the relationships of C-Reactive Protein (CRP, inflammation biomarker) with clinical symptoms and reward-related brain activation.MethodsSubjects were 64 psychotropic-medication-free adolescents with psychiatric symptoms (ages: 15.17 ± 2.10, 44 female). All had psychiatric evaluations and dimensional assessments for anxiety, depression, anhedonia, and suicidality. Neuroimaging included the Reward Flanker fMRI Task examining brain activation during reward anticipation, attainment and positive prediction error. Both whole-brain and ROI analyses focusing on reward circuitry were performed. All analyses were controlled for BMI, age, and sex at pFWE < 0.05.ResultsNo relationships were identified between CRP and clinical symptom severity. CRP was positively associated with brain activation during reward attainment in regions of the visual and dorsal attention networks, as well as during positive prediction error in the cerebellum. In ROI analyses, CRP was negatively correlated with brain activation during reward anticipation in dorsal anterior cingulate cortex. When subject with high CRP was excluded, CRP was also positively correlated with positive predication error activation in nucleus accumbens.ConclusionDespite lack of associations of CRP with clinical symptomatology, our fMRI findings suggest a relationship between inflammation and brain function early course of psychiatric conditions.
| S-EPMC7771888 | biostudies-literature
Project description:ObjectivesEarly life stress likely contributes to dysfunction in neural reward processing systems. However, studies to date have focused almost exclusively on adolescents and adults, measured early life stress retrospectively, and have often failed to control for concurrent levels of stress. The current study examined the contribution of prospectively measured cumulative life stress in preschool-age children on reward-related neural activation and connectivity in school-age children.MethodsChildren (N = 46) and caregivers reported children's exposure to early life stress between birth and preschool age (mean = 4.8 years, SD = 0.80). At follow-up (mean age = 7.52 years, SD = .78), participants performed a child-friendly monetary incentive delay task during functional magnetic resonance imaging.ResultsChildren with higher levels of cumulative early life stress, controlling for concurrent stressful life events, exhibited aberrant patterns of neural activation and connectivity in reward- and emotion-related regions (e.g., prefrontal cortex, temporal pole, culmen), depending on the presence of a potential reward and whether or not the target was hit or missed.ConclusionsFindings suggest that stress exposure during early childhood may impact neural reward processing systems earlier in development than has previously been demonstrated. Understanding how early life stress relates to alterations in reward processing could guide earlier, more mechanistic interventions.
| S-EPMC8144345 | biostudies-literature
Project description:Compared to our understanding of positive prediction error signals occurring due to unexpected reward outcomes, less is known about the neural circuitry in humans that drives negative prediction errors during omission of expected rewards. While classical learning theories such as Rescorla-Wagner or temporal difference learning suggest that both types of prediction errors result from a simple subtraction, there has been recent evidence suggesting that different brain regions provide input to dopamine neurons which contributes to specific components of this prediction error computation. Here, we focus on the brain regions responding to negative prediction error signals, which has been well-established in animal studies to involve a distinct pathway through the lateral habenula. We examine the activity of this pathway in humans, using a conditioned inhibition paradigm with high-resolution functional MRI. First, participants learned to associate a sensory stimulus with reward delivery. Then, reward delivery was omitted whenever this stimulus was presented simultaneously with a different sensory stimulus, the conditioned inhibitor (CI). Both reward presentation and the reward-predictive cue activated midbrain dopamine regions, insula and orbitofrontal cortex. While we found significant activity at an uncorrected threshold for the CI in the habenula, consistent with our predictions, it did not survive correction for multiple comparisons and awaits further replication. Additionally, the pallidum and putamen regions of the basal ganglia showed modulations of activity for the inhibitor that did not survive the corrected threshold.
| S-EPMC7928384 | biostudies-literature
Project description:ObjectiveAlthough 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.MethodThe 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.ResultsOur 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.ConclusionMultimodal 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.
| S-EPMC8643367 | biostudies-literature
Project description:Individuals involved in antisocial behavior often engage in excessive reward-driven behavior even in the face of severe punishments including incarceration. However, the neural mechanisms of reward processing in antisocial behavior have not been examined while considering the heterogeneity of antisocial behavior and specific phases of reward and loss processing. In this study, we investigate the relationship between antisocial behavior, callous-unemotional traits, and neural activity during the anticipation and receipt of rewards and losses.A community sample of 144 low income, racially diverse, urban males at risk for antisocial behavior completed self-report measures, a clinical interview, and an fMRI scan at age 20. Neural response during the anticipation and receipt of monetary rewards and losses was linked to antisocial behavior and callous-unemotional traits using a priori ventral striatum region of interest analyses and exploratory whole brain analyses.Antisocial behavior, but not callous-unemotional traits, was related to less ventral striatum response during reward anticipation. There were no significant relationships between neural reactivity and antisocial behavior or callous-unemotional traits during reward or loss outcomes. Antisocial behavior was also related to less ventrolateral prefrontal cortex reactivity during reward and loss anticipation.These findings support a hypo-reactivity model of reward and loss anticipation in antisocial behavior. Lower striatal reactivity to cues of reward and lower prefrontal-regulatory recruitment during reward and loss anticipation may contribute to maladaptive reward-related behavior found in antisocial behavior.
| S-EPMC5606223 | biostudies-literature
Project description:This study aimed to characterize the role of sex and pubertal markers in reward motivation behavior and neural processing in early adolescence. We used baseline and two-year follow-up data from the Adolescent Brain and Cognitive DevelopmentSM study (15844 observations; 52% from boys; age 9-13). Pubertal development was measured with parent-reported Pubertal Development Scale, and DHEA, testosterone, and estradiol levels. Reward motivation behavior and neural processing at anticipation and feedback stages were assessed with the Monetary Incentive Delay task. Boys had higher reward motivation than girls, demonstrating greater accuracy difference between reward and neutral trials and higher task earnings. Girls had lower neural activation during reward feedback than boys in the nucleus accumbens, caudate, rostral anterior cingulate, medial orbitofrontal cortex, superior frontal gyrus and posterior cingulate. Pubertal stage and testosterone levels were positively associated with reward motivation behavior, although these associations changed when controlling for age. There were no significant associations between pubertal development and neural activation during reward anticipation and feedback. Sex differences in reward-related processing exist in early adolescence, signaling the need to understand their impact on typical and atypical functioning as it unfolds into adulthood.
| S-EPMC10904160 | biostudies-literature
Project description:Drinking water is innately rewarding to thirsty animals. In addition, the consumed value can be assigned to behavioral actions and predictive sensory cues by associative learning. Here we show that thirst converts water avoidance into water-seeking in naive Drosophila melanogaster. Thirst also permitted flies to learn olfactory cues paired with water reward. Water learning required water taste and <40 water-responsive dopaminergic neurons that innervate a restricted zone of the mushroom body ? lobe. These water learning neurons are different from those that are critical for conveying the reinforcing effects of sugar. Naive water-seeking behavior in thirsty flies did not require water taste but relied on another subset of water-responsive dopaminergic neurons that target the mushroom body ?' lobe. Furthermore, these naive water-approach neurons were not required for learned water-seeking. Our results therefore demonstrate that naive water-seeking, learned water-seeking and water learning use separable neural circuitry in the brain of thirsty flies.
| S-EPMC4213141 | biostudies-literature