Aberrant Disgust Responses and Immune Reactivity in Cocaine-Dependent Men

Background: Infectious diseases are the most common and cost-intensive health complications associated with drug addiction. There is wide belief that drug-dependent individuals expose themselves more regularly to disease-related pathogens through risky behaviors such as sharing pipes and needles, thereby increasing their risk for contracting an infectious disease. However, evidence is emerging indicating that not only lifestyle but also the immunomodulatory effects of addictive drugs, such as cocaine, may account for their high infection risk. As feelings of disgust are thought to be an important psychological mechanism in avoiding the exposure to pathogens, we sought to investigate behavioral, physiological, and immune responses to disgust-evoking cues in both cocaine-dependent and healthy men. Methods: All participants (N = 61) were exposed to neutral and disgust-evoking photographs depicting food and nonfood images while response accuracy, latency, and skin conductivity were recorded. Saliva samples were collected before and after exposure to neutral and disgusting images, respectively. Attitudes toward disgust and hygiene behaviors were assessed using questionnaire measures. Results: Response times to disgust-evoking photographs were prolonged in all participants, and specifically in cocaine-dependent individuals. While viewing the disgusting images, cocaine-dependent individuals exhibited aberrant skin conductivity and increased the secretion of the salivary cytokine interleukin-6 relative to control participants. Conclusion: Our data provide evidence of a hypersensitivity to disgusting stimuli in cocaine-dependent individuals, possibly reflecting conditioned responses to noningestive sources of infection. Coupled with a lack of interoception of bodily signals, aberrant disgust responses might lead to increased infection susceptibility in affected individuals

Aberrant Neural Function During Emotion Attribution in Female Subjects With Fragile X Syndrome

Objective: Fragile X (FraX) syndrome is caused by mutations of the FraX mental retardation-1 gene—a gene responsible for producing FraX mental retardation protein. The neurocognitive phenotype associated with FraX in female subjects includes increased risk for emotional disorders including social anxiety, depression, and attention deficit. Here, the authors investigated the neurobiological systems underlying emotion attribution in female subjects with FraX syndrome. Method: While undergoing functional magnetic resonance imaging, 10 high-functioning female subjects with FraX syndrome and 10 typically developing (TD) female subjects were presented with photographs of happy, sad, and neutral faces and instructed to determine the facial emotion. Results: No significant group differences were found for the recognition of happy faces, although the FraX group showed a trend toward a significant difference for the recognition of sad faces and significantly poorer recognition of neutral faces. Controlling for between-group differences in IQ and performance accuracy, the TD group had greater activation than the FraX group in the anterior cingulate cortex (ACC) for neutral faces compared with scrambled faces and the caudate for sad faces compared with scrambled faces (but not for sad faces compared with neutral faces). In the FraX group, FraX mental retardation protein levels positively correlated with activation in the dorsal ACC for neutral, happy, and sad faces when independently compared with scrambled faces. Significantly greater negative correlation between IQ and insula activation for neutral faces relative to scrambled faces was observed in the FraX group compared with the TD group. Significantly greater positive correlation between IQ and ACC activation for neutral faces relative to scrambled faces was observed in the TD group compared with the FraX group. Conclusions: Although emotion recognition is generally spared in FraX syndrome, the emotion circuit (i.e., ACC, caudate, insula) that modulates emotional responses to facial stimuli may be disrupted

Cortical thickness, surface area, and folding alterations in male youths with conduct disorder and varying levels of callous-unemotional traits

Purpose: previous studies have reported changes in gray matter volume in youths with conduct disorder (CD), although these differences are difficult to interpret as they may have been driven by alterations in cortical thickness, surface area (SA), or folding. The objective of this study was to use surface-based morphometry (SBM) methods to compare male youths with CD and age and sex-matched healthy controls (HCs) in cortical thickness, SA, and folding. We also tested for structural differences between the childhood-onset and adolescence-onset subtypes of CD and performed regression analyses to assess for relationships between CD symptoms and callous-unemotional (CU) traits and SBM-derived measures. Methods: we acquired structural neuroimaging data from 20 HC and 36 CD participants (18 with childhood-onset CD and 18 with adolescence-onset CD) and analysed the data using FreeSurfer. Results: relative to HCs, youths with CD showed reduced cortical thickness in the superior temporal gyrus, reduced SA in the orbitofrontal cortex (OFC), and increased cortical folding in the insula. There were no significant differences between the childhood-onset and adolescence-onset CD subgroups in cortical thickness or SA, but several frontal and temporal regions showed increased cortical folding in childhood-onset relative to adolescence-onset CD participants. CD symptoms were negatively correlated with OFC SA whereas CU traits were positively correlated with insula folding.Conclusions: cortical thinning in the superior temporal gyrus may contribute to the social cognitive impairments displayed by youths with CD, whereas reduced OFC SA may lead to impairments in emotion regulation and reward processing in youths with CD. The increased cortical folding observed in the insula may reflect a maturational delay in this region and could mediate the link between CU traits and empathy deficits. Altered cortical structure was observed in childhood-onset and adolescence-onset forms of C

Cortical thickness, surface area, and folding alterations in male youths with conduct disorder and varying levels of callous-unemotional traits.

PURPOSE: Previous studies have reported changes in gray matter volume in youths with conduct disorder (CD), although these differences are difficult to interpret as they may have been driven by alterations in cortical thickness, surface area (SA), or folding. The objective of this study was to use surface-based morphometry (SBM) methods to compare male youths with CD and age and sex-matched healthy controls (HCs) in cortical thickness, SA, and folding. We also tested for structural differences between the childhood-onset and adolescence-onset subtypes of CD and performed regression analyses to assess for relationships between CD symptoms and callous-unemotional (CU) traits and SBM-derived measures. METHODS: We acquired structural neuroimaging data from 20 HCs and 36 CD participants (18 with childhood-onset CD and 18 with adolescence-onset CD) and analyzed the data using FreeSurfer. RESULTS: Relative to HCs, youths with CD showed reduced cortical thickness in the superior temporal gyrus, reduced SA in the orbitofrontal cortex (OFC), and increased cortical folding in the insula. There were no significant differences between the childhood-onset and adolescence-onset CD subgroups in cortical thickness or SA, but several frontal and temporal regions showed increased cortical folding in childhood-onset relative to adolescence-onset CD participants. Both CD subgroups also showed increased cortical folding relative to HCs. CD symptoms were negatively correlated with OFC SA whereas CU traits were positively correlated with insula folding. CONCLUSIONS: Cortical thinning in the superior temporal gyrus may contribute to the social cognitive impairments displayed by youths with CD, whereas reduced OFC SA may lead to impairments in emotion regulation and reward processing in youths with CD. The increased cortical folding observed in the insula may reflect a maturational delay in this region and could mediate the link between CU traits and empathy deficits. Altered cortical folding was observed in childhood-onset and adolescence-onset forms of CD.This study was supported by Wellcome Trust project grant 083140 (Drs. Goodyer and Fairchild), Medical Research Council project code MC_US_A060_5PQ50 (Dr. Calder), and the Betty Behrens Research Fellowship at Clare Hall, Cambridge University (Dr. Passamonti). The authorswould like to thank the participants and their families for taking part in this study, as well as the Cambridge Youth Offending Service for their help with recruitment.This is the final version. It was first published by Elsevier at http://www.sciencedirect.com/science/article/pii/S2213158215000856

Seven Computations of the Social Brain

The social environment presents the human brain with the most complex of information processing demands. The computations that the brain must perform occur in parallel, combine social and nonsocial cues, produce verbal and non-verbal signals, and involve multiple cognitive systems; including memory, attention, emotion, learning. This occurs dynamically and at timescales ranging from milliseconds to years. Here, we propose that during social interactions, seven core operations interact to underwrite coherent social functioning; these operations accumulate evidence efficiently – from multiple modalities – when inferring what to do next. We deconstruct the social brain and outline the key components entailed for successful human social interaction. These include (1) social perception; (2) social inferences, such as mentalizing; (3) social learning; (4) social signaling through verbal and non-verbal cues; (5) social drives (e.g., how to increase one’s status); (6) determining the social identity of agents, including oneself; and (7) minimizing uncertainty within the current social context by integrating sensory signals and inferences. We argue that while it is important to examine these distinct aspects of social inference, to understand the true nature of the human social brain, we must also explain how the brain integrates information from the social world

Reflected glory and failure: the role of the medial prefrontal cortex and ventral striatum in self vs other relevance during advice-giving outcomes

Despite the risks, people enjoy giving advice. One explanation is that giving beneficial advice can result in reflected glory, ego boosts or reputation enhancement. However, giving poor advice can be socially harmful (being perceived as incompetent or untrustworthy). In both circumstances, we have a vested interest in the advice follower's success or failure, especially when it reflects specifically on us compared with when it is diffused between multiple advisors. We examined these dynamics using an Advisor-Advisee Game, where subjects acted as an Advisor to a confederate Advisee who selected one of the three options when trying to win money: accept the subject's advice, accept the advice of a second confederate Advisor or accept both Advisors' advice. Results showed that having one's advice accepted, compared with being rejected, resulted in activity in the ventral striatum--a core reward area. Furthermore, the ventral striatum was only active when the subject's advice led to the advisee winning, and not when the advisee won based on the confederate's advice. Finally, the medial prefrontal cortex (MPFC) was more active when the Advisee won or lost money based solely on the subject's advice compared with when the second Advisor's advice was accepted. One explanation for these findings is that the MPFC monitors self-relevant social information, while the ventral striatum is active when others accept advice and when their success leads to reflected glory

Neurodevelopment and ages of onset in depressive disorders

How and why do clinical depressive disorders emerge in adolescence? In this Personal View, we present a neurodevelopmental theory to address causes for adolescent onsets of clinical depressive disorders. We argue that theories should account for three perplexing aspects of depressive disorders in adolescence: the episodic nature of depression; differences between sexes in rates of depression across development; and age-differentiated onsets. We consider how theories such as psychosocial acceleration, heterochronic brain development, dual-process models, glucocorticoid vulnerability hypothesis linked to early life stress, and epigenetic and genetic susceptibility might explain some aspects of adolescent depressive disorders. We argue that some synthesis between existing theories might be needed to establish a sufficient neurodevelopmental theoretical framework to explain onsets of depressive disorders in adolescence