Chemogenetic manipulation of the bed nucleus of the stria terminalis counteracts social behavioral deficits induced by early life stress in C57BL/6J mice.

Trauma during critical periods of development can induce long-lasting adverse effects. To study neural aberrations resulting from early life stress (ELS), many studies utilize rodent maternal separation, whereby pups are intermittently deprived of maternal care necessary for proper development. This can produce adulthood behavioral deficits related to anxiety, reward, and social behavior. The bed nucleus of the stria terminalis (BNST) encodes aspects of anxiety-like and social behaviors, and also undergoes developmental maturation during the early postnatal period, rendering it vulnerable to effects of ELS. Mice underwent maternal separation (separation 4 hr/day during postnatal day (PD)2-5 and 8 hr/day on PD6-16) with early weaning on PD17, which induced behavioral deficits in adulthood performance on two-part social interaction task designed to test social motivation (choice between a same-sex novel conspecific or an empty cup) and social novelty preference (choice between the original-novel conspecific vs. a new-novel conspecific). We used chemogenetics to non-selectively silence or activate neurons in the BNST to examine its role in social motivation and social novelty preference, in mice with or without the history of ELS. Manipulation of BNST produced differing social behavior effects in non-stressed versus ELS mice; social motivation was decreased in non-stressed mice following BNST activation, but unchanged following BNST silencing, while ELS mice showed no change in social behavior after BNST activation, but exhibited enhancement of social motivation-for which they were deficient prior-following BNST silencing. Findings emphasize the BNST as a potential therapeutic target for social anxiety disorders instigated by childhood trauma.

Autism spectrum disorder and severe social impairment associated with elevated plasma interleukin-8.

BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disorder with an unclear etiology and pathophysiology. Previous studies have indicated that the dysregulation of cytokines may be involved in the pathogenesis of ASD and that the levels of cytokines may serve as potential biomarkers of this disorder. METHODS: The current study employed a family triad-based case-control design to study the levels of plasma cytokines in families with ASD (n = 45 triads) and controls (n = 38 triads) with a Human Cytokine Twenty-Five-Plex Kit. The Social Responsiveness Scale (SRS) was used to measure social impairment of ASD children. RESULTS: After controlling for the levels of parental cytokines, we identified that interferon-α (IFN-α), interleukin-7 (IL-7), IL-8, IFN-γ-inducible protein-10, and macrophage inflammatory protein-1ß were associated with ASD, and IL-8 was the only cytokine also associated with the levels of both parental cytokines in the offspring-parents regression analysis and three subdomains of SRS (social awareness, cognition, and motivations) in the children with ASD. The receiver operating characteristic curve showed that the log-transformed IL-8 level discriminated children with autism from controls with an area under the curve of 0.858 (95% confidence interval: 0.777-0.939). CONCLUSIONS: Our study suggests that IL-8 is a potential biomarker for ASD and may be involved in the pathogenesis of ASD. IMPACT: The study suggests that IL-8 is a promising biomarker for ASD and may be involved in the pathogenesis of ASD. Only a very few studies have reported the parental cytokine levels. The significant strength of this article is that we applied the family triad-based approach to explore cytokine levels in families with autism and controls. There are no objective biomarkers, making the accurate diagnosis, prognostic prediction and effective treatment difficult, and our study provides promising results.

Lifelong consequences of brain injuries during development: From risk to resilience.

Traumatic brain injuries in children represent a major public health issue and even relatively mild injuries can have lifelong consequences. However, the outcomes from these injuries are highly heterogeneous, with most individuals recovering fully, but a substantial subset experiencing prolonged or permanent disabilities across a number of domains. Moreover, brain injuries predispose individuals to other kinds of neuropsychiatric and somatic illnesses. Critically, the severity of the injury only partially predicts subsequent outcomes, thus other factors must be involved. In this review, we discuss the psychological, social, neuroendocrine, and autonomic processes that are disrupted following traumatic brain injury during development, and consider the mechanisms the mediate risk or resilience after traumatic brain injury in this vulnerable population.

How should we understand the absence of sex differences in the genetic and environmental origins of antisocial behavior?

Available twin-family data on sex differences in antisocial behavior (ASB) simultaneously suggest that ASB is far more prevalent in males than in females, and that its etiology (i.e. the effects of genes, environments, hormones, culture) does not differ across sex. This duality presents a conundrum: How do we make sense of mean sex differences in ASB if not via differences in genes, environments, hormones, and/or cultures? The current selective review and critique explores possible contributions to these seemingly incompatible sets of findings. We asked whether the presence of sex differences in behavior could be smaller than is typically assumed, or confined to a specific set of behaviors. We also asked whether there might be undetected differences in etiology across sex in twin-family studies. We found little evidence that bias or measurement invariance across sex account for phenotypic sex differences in ASB, but we did identify some key limitations to current twin-family approaches. These included the questionable ability of qualitative sex difference analyses to detect gender norms and prenatal exposure to testosterone, and concerns regarding specific analytic components of quantitative sex difference analyses. We conclude that the male preponderance in ASB is likely to reflect a true sex difference in observed behavior. It was less clear, however, that the genetic and environmental contributions to ASB are indeed identical across sex, as argued by prior twin-family studies. It is our hope that this review will inspire the development of new, genetically-informed methods for studying sex differences in etiology.

Compulsive Social Behavior Emerges after Selective Ablation of Striatal Cholinergic Interneurons.

The mechanisms underlying social dysfunction in neuropsychiatric conditions such as obsessive-compulsive disorder and Tourette syndrome remain uncertain. However, it is known that dysfunctions in basal ganglia, including a reduced number of striatal cholinergic interneurons (SCIN), are involved in their pathophysiology. To explore the role of SCIN in relation to perseverative behaviors, we characterized a new transgenic mouse model in which inducible ablation of SCIN is achieved with high efficiency in a cell-type- and region-specific manner. Mice were subjected to extensive behavioral testing, including assessment of social behaviors, and corticostriatal functional connectivity was evaluated in vivo Selective SCIN ablation leads to altered social interactions together with exacerbated spontaneously emitted repetitive behaviors. Lesioned mice showed normal motor coordination, balance, and general locomotion. Interestingly, only environmentally driven, but not self-directed, repetitive behaviors were exacerbated in lesioned mice. Remarkably, in mice with SCIN ablation, the normal pattern of social exploration was replayed continuously. The emerging pattern of social interactions is highly predictable and invariant across time. In vivo electrophysiological recordings indicate that SCIN ablation results in an increase of the functional connectivity between different cortical areas and the motor, but not associative, region of the striatum. Our results identify a role of SCIN in suppressing perseverative behaviors, including socially related ones. In sum, SCIN ablation in mice leads to exacerbated ritualistic-like behaviors that affect social performance, providing a link between SCIN dysfunction and the social impairments present in psychiatric disorders.SIGNIFICANCE STATEMENT We sought to uncover the impact of striatal cholinergic interneuron (SCIN) degeneration on perseverative behaviors related to obsessive-compulsive disorder (OCD) and Tourette syndrome (TS). We found that extensive SCIN ablation results in exacerbated social interactions, in which normal social contacts were replayed continuously in a highly stereotyped, ritualistic pattern. SCIN ablation also leads to an increase in other spontaneously emitted repetitive behaviors without alteration of motor coordination, balance, or locomotion. Moreover, we identify an increase of functional connectivity between frontal cortical areas and the motor region of the striatum as a putative substrate for the observed behavioral alterations. Therefore, perseveration induced by SCIN ablation extends to social performance as occurs in neuropsychiatric conditions such as OCD and TS.

Prospective test of the developmental propensity model of antisocial behavior: from childhood and adolescence into early adulthood.

BACKGROUND: The developmental propensity model of antisocial behavior posits that several dispositional characteristics of children transact with the environment to influence the likelihood of learning antisocial behavior across development. Specifically, greater dispositional negative emotionality, greater daring, and lower prosociality-operationally, the inverse of callousness- and lower cognitive abilities are each predicted to increase risk for developing antisocial behavior. METHODS: Prospective tests of key predictions derived from the model were conducted in a high-risk sample of 499 twins who were assessed on dispositions at 10-17 years of age and assessed for antisocial personality disorder (APD) symptoms at 22-31 years of age. Predictions were tested separately for parent and youth informants on the dispositions using multiple regressions that adjusted for oversampling, nonresponse, and clustering within twin pairs, controlling demographic factors and time since the first assessment. RESULTS: Consistent with predictions, greater numbers of APD symptoms in adulthood were independently predicted over a 10-15 year span by higher youth ratings on negative emotionality and daring and lower youth ratings on prosociality, and by parent ratings of greater negative emotionality and lower prosociality. A measure of working memory did not predict APD symptoms. CONCLUSIONS: These findings support future research on the role of these dispositions in the development of antisocial behavior.

Cognitive behavioural therapy for aggression among individuals with moderate to severe acquired brain injury: a systematic review and meta-analysis.

BACKGROUND: Aggression is common after an acquired brain injury (ABI). Cognitive behavioural therapy (CBT) is a form of psychotherapy, in which therapists help patients to identify their maladaptive behaviours. OBJECTIVE: The objective of this systematic review and meta-analysis was to evaluate the effectiveness of CBT interventions in treating aggression in an ABI population. METHODS: A systematic literature search was conducted using: PubMed/MEDLINE, CINAHL, EMBASE and PsycINFO from database inception to August 2016. English articles were included if: at least 50% of the study sample had a moderate to severe ABI, there were at least three adult human participants, and use of a CBT intervention for the treatment of aggression. RESULTS: Seven articles met inclusion criteria: one RCT, an RCT crossover and five pre-post trials. Of these, four articles were included in a pre-post meta-analysis for treatment efficacy on subscales of the State Trait Anger Expression Inventory (STAXI) and STAXI-2 outcome measures. The meta-analysis found CBT was effective in moderating the external behaviours of aggression, but not internal anger. CONCLUSION: The differences in outcomes may be related to the differential management of anger expression and anger suppression. CBT shows promise, but further studies with comparator groups are needed before conclusions about its efficacy can be made.

Neuropsychiatric Symptoms in Mild Cognitive Impairment.

OBJECTIVE: Neuropsychiatric symptoms (NPS) may be the first manifestation of an underlying neurocognitive disorder. We undertook a review to provide an update on the epidemiology and etiological mechanisms of NPS that occur in mild cognitive impairment (MCI) and just before the onset of MCI. We discuss common clinical presentations and the implications for diagnosis and care. METHOD: The authors conducted a selective review of the literature regarding the emergence of NPS in late life, before and after the onset of MCI. We discuss recent publications that explore the epidemiology and etiological mechanisms of NPS in the earliest clinical stages of these disorders. RESULTS: NPS have been reported in 35% to 85% of adults with MCI and also occur in advance of cognitive decline. The occurrence of NPS for the first time in later life should increase suspicion for an underlying neurocognitive disorder. The presenting symptom may provide a clue regarding the etiology of the underlying disorder, and the co-occurrence of NPS may herald a more accelerated cognitive decline. CONCLUSIONS: NPS are prevalent in the early clinical stages of neurocognitive disorders and can serve as both useful diagnostic and prognostic indicators. Recognition of NPS as early manifestations of neurocognitive disorders will become increasingly important as we move towards preventative strategies and disease-modifying treatments that may be most effective when deployed in the earliest stages of disease.

Functional changes of the reward system underlie blunted response to social gaze in cocaine users.

Social interaction deficits in drug users likely impede treatment, increase the burden of the affected families, and consequently contribute to the high costs for society associated with addiction. Despite its significance, the neural basis of altered social interaction in drug users is currently unknown. Therefore, we investigated basal social gaze behavior in cocaine users by applying behavioral, psychophysiological, and functional brain-imaging methods. In study I, 80 regular cocaine users and 63 healthy controls completed an interactive paradigm in which the participants' gaze was recorded by an eye-tracking device that controlled the gaze of an anthropomorphic virtual character. Valence ratings of different eye-contact conditions revealed that cocaine users show diminished emotional engagement in social interaction, which was also supported by reduced pupil responses. Study II investigated the neural underpinnings of changes in social reward processing observed in study I. Sixteen cocaine users and 16 controls completed a similar interaction paradigm as used in study I while undergoing functional magnetic resonance imaging. In response to social interaction, cocaine users displayed decreased activation of the medial orbitofrontal cortex, a key region of reward processing. Moreover, blunted activation of the medial orbitofrontal cortex was significantly correlated with a decreased social network size, reflecting problems in real-life social behavior because of reduced social reward. In conclusion, basic social interaction deficits in cocaine users as observed here may arise from altered social reward processing. Consequently, these results point to the importance of reinstatement of social reward in the treatment of stimulant addiction.

Different brain responses during empathy in autism spectrum disorders versus conduct disorder and callous-unemotional traits.

BACKGROUND: Deficits in empathy are reported in autism spectrum disorders (ASD) and also underlie antisocial behavior of individuals with conduct disorder and callous-unemotional traits (CD/CU+). Many studies suggest that individuals with ASD are typically impaired in cognitive aspects of empathy, and individuals with CD/CU+ typically in affective aspects. In the current study, we compared the neural correlates of cognitive and affective aspects of empathy between youth with ASD and youth with CD/CU+. METHODS: Functional magnetic resonance imaging (fMRI) was used to assess boys with ASD (N = 23), boys with CD/CU+ (N = 23), and typically developing (TD) boys (N = 33), aged 15-19 years. Angry and fearful faces were presented and participants were asked to either infer the emotional state from the face (other-task; emotion recognition) or to judge their own emotional response to the face (self-task; emotional resonance). RESULTS: During emotion recognition, boys with ASD showed reduced responses compared to the other groups in the ventromedial prefrontal cortex (vmPFC). During emotional resonance, the CD/CU+ and ASD groups showed reduced amygdala responses compared to the TD controls, boys with ASD showed reduced responses in bilateral hippocampus, and the CD/CU+ boys showed reduced responses in the inferior frontal gyrus (IFG) and anterior insula (AI). CONCLUSION: Results suggest differential abnormal brain responses associated with specific aspects of empathic functioning in ASD and CD/CU+. Decreased amygdala responses in ASD and CD/CU+ might point to impaired emotion processing in both disorders, whereas reduced vmPFC responses suggest problems in processing cognitive aspects of empathy in ASD. Reduced IFG/AI responses, finally, suggest decreased emotional resonance in CD/CU+.

Schizophrenia and reelin: a model based on prenatal stress to study epigenetics, brain development and behavior.

Schizophrenia is a severe psychiatric disorder that results in a significant disability for the patient. The disorder is characterized by impairment of the adaptive orchestration of actions, a cognitive function that is mainly dependent on the prefrontal cortex. This behavioral deficit, together with cellular and neurophysiological alterations in the prefrontal cortex, as well as reduced density of GABAergic cells and aberrant oscillatory activity, all indicate structural and functional deficits of the prefrontal cortex in schizophrenia. Among the several risk factors for the development of schizophrenia, stress during the prenatal period has been identified as crucial. Thus, it is proposed that prenatal stress induces neurodevelopmental alterations in the prefrontal cortex that are expressed as cognitive impairment observed in schizophrenia. However, the precise mechanisms that link prenatal stress with the impairment of prefrontal cortex function is largely unknown. Reelin is an extracellular matrix protein involved in the development of cortical neural connectivity at embryonic stages, and in synaptic plasticity at postnatal stages. Interestingly, down-regulation of reelin expression has been associated with epigenetic changes in the reelin gene of the prefrontal cortex of schizophrenic patients. We recently showed that, similar to schizophrenic patients, prenatal stress induces down-expression of reelin associated with the methylation of its promoter in the rodent prefrontal cortex. These alterations were paralleled with altered prefrontal cortex functional connectivity and impairment in prefrontal cortex-dependent behavioral tasks. Therefore, considering molecular, cellular, physiological and behavioral evidence, we propose a unifying framework that links prenatal stress and prefrontal malfunction through epigenetic alterations of the reelin gene.

Social-emotional instability in individuals with Rett syndrome: parents' experiences with second stage behaviour.

BACKGROUND: While the medical profession often terms behaviours in individuals with Rett syndrome (RTT) in the second stage as 'autistic-like', parents disagree with this description. The present study focuses on a comparison of parents' experiences with the social-emotional behaviour of the child with RTT in the second and subsequent stages. METHOD: In collaboration with the Dutch Rett Syndrome Organization, 51 parents of children with RTT in the Netherlands took part in the present study. Parents completed an online questionnaire to clarify their experiences of the social-emotional behaviour of their children during and after the second stage of RTT. Both quantitative and qualitative analysis techniques have been used. RESULTS: The results of the paired-samples t-test show that parents see significantly less social-emotional behaviour in the children during the second stage of RTT than in the subsequent stages. Parents reported that their children did not seek as much interaction. From the parents' descriptions, it would seem that the children are willing but unable to interact with their environment. CONCLUSIONS: Like previous research, our study leads to doubts about the appropriateness of the label 'autistic-like' for the behaviour of individuals in the second stage of RTT. While behaviours of individuals with autism and individuals with RTT may resemble each other, quality and intentions may differ. Still, future studies are needed for further clarification.

Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development.

BACKGROUND: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. METHOD: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. RESULTS: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. CONCLUSIONS: Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression.

[Association between serotonin receptor 2C gene Cys23Ser polymorphism and social behavior in schizophrenia patients and healthy individuals].

The purpose of this work was to search for associations between the serotonin receptor 2C gene (HTR2C) and the peculiarities of social behavior and social cognition in schizophrenia. To do this, patients with schizophrenia spectrum disorders and healthy control subjects were genotyped for the Cys23Ser HTR2C marker and underwent psychological examination, including assessment of Machiavellianism, recognition of emotions in facial expression, and theory of mind. In addition, we estimated the trait anxiety level as a potential factor affecting the relationship between the gene HTR2C and social behavior. We found a significant association between the Ser allele and a reduction of estimates on the Mach-LV Machiavellianism scale in the total sample of patients (n = 182) and control subjects (n = 189), which did not reach the confidence level in either of the groups. A tendency towards a HTR2C gene influence on the trait anxiety level was also revealed. The association between HTR2C and Machiavellianism was retained if the anxiety level was taken into account. The results suggest a pleiotropic effect of HTR2Con anxiety and Machiavellianism.

A longitudinal examination of psychosocial impairment across the anxiety disorders.

BACKGROUND: Anxiety disorders are highly prevalent disorders associated with substantial psychosocial impairment, but few studies have examined impairment within specific anxiety disorders. Furthermore, it is unclear how change in different types of anxiety has an impact on change in impairment, particularly given high rates of co-morbidity. The current study assessed the temporal associations of impairment and symptoms of three common anxiety disorders in a large, diagnostically heterogeneous clinical sample. METHOD: Data were collected from 606 treatment-seeking individuals at an anxiety clinic, most of whom subsequently enrolled in cognitive-behavioral therapy. Symptoms of panic, social anxiety and generalized anxiety disorder (GAD), as well as levels of impairment, were assessed three times over 2 years. In addition to examining levels of impairment across diagnostic groups, latent growth modeling was used to evaluate the longitudinal associations of anxiety symptoms and impairment. RESULTS: Those with a principal diagnosis of GAD reported higher levels of impairment in some domains at baseline; however, at follow-up assessments individuals with social anxiety disorder reported greater impairment than those with panic disorder. Anxiety symptoms and impairment both declined over time. Change in all three anxiety symptoms was closely associated with change in impairment, but only GAD remained a significant (positive) predictor of change in impairment after accounting for co-morbidity. CONCLUSIONS: Impairment and all three anxiety disorders were closely associated, both cross-sectionally and longitudinally. Because change in GAD was most specifically related to change in impairment, treatment for those with multiple anxiety disorders could focus on treating GAD symptoms first or treating transdiagnostic processes.

Antisocial behaviour and lying: a neuropsychiatric presentation of agenesis of the corpus callosum.

OBJECTIVE: The purpose of this case study is to describe the case of a person with agenesis of the corpus callosum (ACC), intellectual disability and features of antisocial behaviour and lying. METHODS: A 26-year-old woman with a mild intellectual disability who presented with antisocial behaviour and chronic lying was found to have ACC and associated cerebral abnormalities. RESULTS: Psychiatric, radiological and neuropsychological assessment of this patient provided convergent evidence of the importance of the corpus callosum in enabling understanding of social situations and appropriate social behaviour, particularly via its connectivity with the frontal regions of the brain. CONCLUSION: Antisocial behaviour and lying may be more commonly associated with callosal dysgenesis than is currently realised.

Pragmatic deficits and social impairment in children with ADHD.

BACKGROUND: Impaired social functioning has been well documented in individuals with attention-deficit/hyperactivity disorder (ADHD). Existing treatments for ADHD are effective for managing core symptoms, but have limited effectiveness at improving social skills, suggesting that social deficits in ADHD may not be directly related to core symptoms of the disorder. Language problems are also common in ADHD, with accumulating evidence of pragmatic language difficulties. Pragmatic deficits are associated with social impairment in several neurodevelopmental disorders. This study systematically examined pragmatic language functioning in children with ADHD and whether social impairment in ADHD is mediated by pragmatic deficits. METHOD: Sixty-three children (28 ADHD; 35 typically developing), ages 7-11 years, underwent a comprehensive assessment of pragmatic language, including parent ratings, standardized tests, and a narrative task. Parents also rated children's social skills on the Social Skills Improvement System. RESULTS: Children with ADHD had poorer pragmatic language skills relative to peers across all measures, even after controlling for general language abilities. Furthermore, pragmatic abilities as measured by parent ratings, mediated the relation between ADHD and social skills. CONCLUSIONS: Pragmatic language skills are impaired in many children with ADHD and may partially account for high rates of social impairment. Implications for treatment and possible prevention of social problems in children with ADHD are discussed.

Behavioural phenotypes of the mucopolysaccharide disorders: a systematic literature review of cognitive, motor, social, linguistic and behavioural presentation in the MPS disorders.

BACKGROUND: The mucopolysaccharide disorders (MPS) are a group of recessively inherited metabolic disorders resulting in progressive physical and cognitive decline. MATERIALS AND METHODS: MEDLINE, PsycINFO and Embase databases were searched, alongside manual screening, to identify relevant literature. Papers were included in the review if they were published in a peer reviewed journal and conducted empirical research into cognitive, motor, social or linguistic development or behaviour in one or more MPS disorders. RESULTS: Twenty-five papers were reviewed. Two papers used methodology of a sufficiently high standard to demonstrate a behavioural phenotype; both found sleep disturbance to be part of the phenotype of MPS III. Fearfulness and sleep disturbance were frequently observed in people with MPS I and II. Cognitive and motor impairment and decline, and challenging behaviour were highly prevalent in the severe form of MPS II. Cognitive decline and severe behavioural problems relating to aggression, hyperactivity, orality, unusual affect and temper tantrums were seen in MPS III. CONCLUSIONS: Sleep disturbance is part of the behavioural phenotype of MPS III, and challenging behaviour is highly prevalent in MPS II and MPS III, therefore the efficacy of behavioural interventions for these populations should be investigated. Further research into the behaviour and adaptive skills of children with MPS III and MPS IV is required.

Alcohol-related cues reduce cognitive control in social drinkers.

Alcohol-related stimuli attract social drinkers' attention (attentional bias). We devised a dual task to test whether attentional biases to alcohol-related stimuli are modulated by cognitive control mechanisms. Sixteen nondependent healthy social drinkers were required to respond to the direction of a central arrow (target) and to ignore adjacent congruent (low cognitive load) or incongruent (high cognitive load) distracting arrows (flankers) in the presence of alcohol-related, neutral or plain grey backgrounds. Percentages of correct responses to the target and reaction time of correct responses (latency) were recorded. The difference score of the flanker effect (latency incongruent-latency congruent) between trials when backgrounds were alcohol-related relative to when they were neutral was also computed. Latencies increased in the presence of the alcohol-related images relative to both the neutral and the grey displays, but only under high cognitive load. Response accuracy did not show this significant difference. The flanker effect difference score correlated positively with the participants' average weekly alcohol intake. The data suggest that the presence of alcohol-associated stimuli attenuates cognitive control processes in social drinkers, an effect that was associated with the participants' average weekly alcohol intake.

Biological motion processing as a hallmark of social cognition.

Visual processing of biological motion (BM) produced by living organisms is of immense value for successful daily-life activities and, in particular, for adaptive social behavior and nonverbal communication. Investigation of BM perception in neurodevelopmental disorders related to autism, preterm birth, and genetic conditions substantially contributes to our understanding of the neural mechanisms underpinning the extraordinary tuning to BM. The most prominent research outcome is that patients with daily-life deficits in social cognition are also compromised on visual body motion processing. This raises the question of whether performance on body motion perception tasks may serve a hallmark of social cognition. Overall, the findings highlight the role of structural and functional brain connectivity for proper functioning of the neural circuitry involved in BM processing and visual social cognition that share topographically and dynamically overlapping neural networks.