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Purpose of Review Personality factors have been implicated in risk for substance use disorders through longitudinal and neurobiologic studies for over four decades. Only recently, however, have targeted interventions been developed to assist individuals with personality risk factors for substance use disorders manage their risk. This article reviews current practices in personality-targeted interventions and the eight randomised trials examining the efficacy of such approaches with respect to reducing and preventing substance use and misuse. Recent Findings Results indicate a moderate mean effect size for personality-targeted approaches across several different substance use outcomes and intervention settings and formats. Conclusions Personality-targeted interventions offer several advantages over traditional substance use interventions, particularly when attempting to prevent development of problems in high-risk individuals or when addressing concurrent mental health problems in brief interventions.

Major neurocognitive changes occur during adolescence, making this phase one of the most critical developmental periods of life. Furthermore, this phase in life is also the time in which youth substance use begins. Several studies have demonstrated the differential associations of alcohol and cannabis use concerning the neurocognitive functioning of both males and females. Past and contemporary literature on gender-specific effects in neuroscience of addiction is predominantly based on cross-sectional datasets and data that is limited in terms of measurement variability. Given the importance of gender-specific effects in addiction studies, and in order to address the two above-mentioned gaps in the literature, the present study aimed to compare neurocognitive functioning of male and female adolescents in the context of cannabis and alcohol use, while employing a longitudinal design with multiple repeated measurements. Participants were 3,826 high school students (47% female; mean age, 12.7), who were recruited from 31 high schools in the greater Montreal area. Participants were requested to complete annual surveys for five consecutive years, from 7th to 11th grade, assessing their alcohol/cannabis use and neurocognitive functioning (working memory, delayed recall memory, perceptual reasoning, and inhibition control). The analytical strategy focused on the longitudinal association between each predictor (female, male) and each of the outcomes (domains of neurocognitive functioning). Multilevel linear models assessed the association of alcohol and cannabis consumption and the four domains of neurocognitive functioning. Results revealed a gender by within-subject interaction, suggesting a weaker effect of yearly fluctuation of cannabis use on working memory among males compared to females. Our findings suggest a different pattern of neurocognitive impairment of female and male working memory after using cannabis over the course of adolescence. Early initiation of cannabis use potentially results in more spatial working memory deficits in female adolescents. This may negatively influence young females' capacity in academic settings and lead to significant impairment in adulthood, which critically decreases the individual's quality of life.

Impulse control is becoming a critical survival skill for the twenty-first century. Impulsivity is implicated in virtually all externalizing behaviours and disorders, and figures prominently in the aetiology and long-term sequelae of substance use disorders (SUDs). Despite its robust clinical and predictive validity, the study of impulsivity is complicated by its multidimensional nature, characterized by a variety of trait-like personality dimensions, as well as by more state-dependent neurocognitive dimensions, with variable convergence across measures. This review provides a hierarchical framework for linking self-report and neurocognitive measures to latent constructs of impulsivity and, in turn, to different psychopathology vulnerabilities, including substance-specific addictions and comorbidities. Impulsivity dimensions are presented as novel behavioural targets for prevention and intervention. Novel treatment approaches addressing domains of impulsivity are reviewed and recommendations for future directions in research and clinical interventions for SUDs are offered. This article is part of the theme issue 'Risk taking and impulsive behaviour: fundamental discoveries, theoretical perspectives and clinical implications'.

Here we report the first and most robust evidence about how sleep habits are associated with regional brain grey matter volumes and school grade average in early adolescence. Shorter time in bed during weekdays, and later weekend sleeping hours correlate with smaller brain grey matter volumes in frontal, anterior cingulate, and precuneus cortex regions. Poor school grade average associates with later weekend bedtime and smaller grey matter volumes in medial brain regions. The medial prefrontal - anterior cingulate cortex appears most tightly related to the adolescents’ variations in sleep habits, as its volume correlates inversely with both weekend bedtime and wake up time, and also with poor school performance. These findings suggest that sleep habits, notably during the weekends, have an alarming link with both the structure of the adolescent brain and school performance, and thus highlight the need for informed interventions.

Playing video games is a common recreational activity of adolescents. Recent research associated frequent video game playing with improvements in cognitive functions. Improvements in cognition have been related to grey matter changes in prefrontal cortex. However, a fine-grained analysis of human brain structure in relation to video gaming is lacking. In magnetic resonance imaging scans of 152 14-year old adolescents, FreeSurfer was used to estimate cortical thickness. Cortical thickness across the whole cortical surface was correlated with self-reported duration of video gaming (hours per week). A robust positive association between cortical thickness and video gaming duration was observed in left dorsolateral prefrontal cortex (DLPFC) and left frontal eye fields (FEFs). No regions showed cortical thinning in association with video gaming frequency. DLPFC is the core correlate of executive control and strategic planning which in turn are essential cognitive domains for successful video gaming. The FEFs are a key region involved in visuo-motor integration important for programming and execution of eye movements and allocation of visuo-spatial attention, processes engaged extensively in video games. The results may represent the biological basis of previously reported cognitive improvements due to video game play. Whether or not these results represent a-priori characteristics or consequences of video gaming should be studied in future longitudinal investigations.

[This corrects the article DOI: 10.3389/fnhum.2020.00095.].[This corrects the article DOI: 10.3389/fnhum.2020.00095.].

Childhood maltreatment (CM) and genetic vulnerability are both risk factors for psychosis, but the relations between them are not fully understood. Guided by the recent identification of genetic risk to CM, this study investigates the hypothesis that genetic risk to schizophrenia also increases the risk of CM and thus impacts psychosis risk. The relationship between schizophrenia polygenetic risk, CM, and psychotic-like experiences (PLE) was investigated in participants from the Utrecht Cannabis Cohort ( N  = 1262) and replicated in the independent IMAGEN cohort ( N  = 1740). Schizophrenia polygenic risk score (SZ-PRS) were calculated from the most recent GWAS. The relationship between CM, PRS, and PLE was first investigated using multivariate linear regression. Next, mediation of CM in the pathway linking SZ-PRS and PLE was examined by structural equation modeling, while adjusting for a set of potential mediators including cannabis use, smoking, and neuroticism. In agreement with previous studies, PLE were strongly associated with SZ-PRS ( B  = 0.190, p  = 0.009) and CM ( B  = 0.575, p  < 0.001). Novel was that CM was also significantly associated with SZ-PRS ( B  = 0.171, p  = 0.001), and substantially mediated the effects of SZ-PRS on PLE (proportion mediated = 29.9%, p  = 0.001). In the replication cohort, the analyses yielded similar results, confirming equally strong mediation by CM (proportion mediated = 34.7%, p  = 0.009). Our results suggest that CM acts as a mediator in the causal pathway linking SZ-PRS and psychosis risk. These findings open new perspectives on the relations between genetic and environmental risks and warrant further studies into potential interventions to reduce psychosis risk in vulnerable people.

A compulsivity spectrum has been hypothesized to exist across Obsessive-Compulsive disorder (OCD), Eating Disorders (ED), substance abuse (SA) and binge-drinking (BD). The objective was to examine the validity of this compulsivity spectrum, and differentiate it from an externalizing behaviors dimension, but also to look at hypothesized personality and neural correlates. A community-sample of adolescents (N=1938; mean age 14.5 years), and their parents were recruited via high-schools in 8 European study sites. Data on adolescents' psychiatric symptoms, DSM diagnoses (DAWBA) and substance use behaviors (AUDIT and ESPAD) were collected through adolescent- and parent-reported questionnaires and interviews. The phenotypic structure of compulsive behaviors was then tested using structural equation modeling. The model was validated using personality variables (NEO-FFI and TCI), and Voxel-Based Morphometry (VBM) analysis. Compulsivity symptoms best fit a higher-order two factor model, with ED and OCD loading onto a compulsivity factor, and BD and SA loading onto an externalizing factor, composed also of ADHD and conduct disorder symptoms. The compulsivity construct correlated with neuroticism (r=0.638; p ≤ 0.001), conscientiousness (r=0.171; p ≤ 0.001), and brain gray matter volume in left and right orbitofrontal cortex, right ventral striatum and right dorsolateral prefrontal cortex. The externalizing factor correlated with extraversion (r=0.201; p ≤ 0.001), novelty-seeking (r=0.451; p ≤ 0.001), and negatively with gray matter volume in the left inferior and middle frontal gyri. Results suggest that a compulsivity spectrum exists in an adolescent, preclinical sample and accounts for variance in both OCD and ED, but not substance-related behaviors, and can be differentiated from an externalizing spectrum.

The firing of mesolimbic dopamine neurons is important for drug-induced reinforcement, although underlying genetic factors remain poorly understood. In a recent genome-wide association metaanalysis of alcohol intake, we identified a suggestive association of SNP rs26907 in the ras-specific guanine-nucleotide releasing factor 2 (RASGRF2) gene, encoding a protein that mediates Ca ²⁺-dependent activation of the ERK pathway. We performed functional characterization of this gene in relation to alcohol-related phenotypes and mesolimbic dopamine function in both mice and adolescent humans. Ethanol intake and preference were decreased in Rasgrf2 ⁻/⁻ mice relative to WT controls. Accordingly, ethanol-induced dopamine release in the ventral striatum was blunted in Rasgrf2 ⁻/⁻ mice. Recording of dopamine neurons in the ventral tegmental area revealed reduced excitability in the absence of Ras-GRF2, likely because of lack of inhibition of the I A potassium current by ERK. This deficit provided an explanation for the altered dopamine release, presumably linked to impaired activation of dopamine neurons firing. Functional neuroimaging analysis of a monetary incentive–delay task in 663 adolescent boys revealed significant association of ventral striatal activity during reward anticipation with a RASGRF2 haplotype containing rs26907, the SNP associated with alcohol intake in our previous metaanalysis. This finding suggests a link between the RASGRF2 haplotype and reward sensitivity, a known risk factor for alcohol and drug addiction. Indeed, follow-up of these same boys at age 16 y revealed an association between this haplotype and number of drinking episodes. Together, these combined animal and human data indicate a role for RASGRF2 in the regulation of mesolimbic dopamine neuron activity, reward response, and alcohol use and abuse.

Background Alcohol misuse amongst young people is a serious concern. The need for effective prevention is clear, yet there appear to be few evidenced-based programs that prevent alcohol misuse and none that target both high and low-risk youth. The CAP study addresses this gap by evaluating the efficacy of an integrated approach to alcohol misuse prevention, which combines the effective universal internet-based Climate Schools program with the effective selective personality-targeted Preventure program. This article describes the development and protocol of the CAP study which aims to prevent alcohol misuse and related harms in Australian adolescents. Methods/Design A cluster randomized controlled trial (RCT) is being conducted with Year 8 students aged 13 to 14-years-old from 27 secondary schools in New South Wales and Victoria, Australia. Blocked randomisation was used to assign schools to one of four groups; Climate Schools only, Preventure only, CAP ( Climate Schools and Preventure ), or Control (alcohol, drug and health education as usual). The primary outcomes of the trial will be the uptake and harmful use of alcohol and alcohol related harms. Secondary outcomes will include alcohol and cannabis related knowledge, cannabis related harms, intentions to use, and mental health symptomatology. All participants will complete assessments on five occasions; baseline; immediately post intervention, and at 12, 24 and 36 months post baseline. Discussion This study protocol presents the design and current implementation of a cluster RCT to evaluate the efficacy of the CAP study; an integrated universal and selective approach to prevent alcohol use and related harms among adolescents. Compared to students who receive the stand-alone universal Climate Schools program or alcohol and drug education as usual (Controls), we expect the students who receive the CAP intervention to have significantly less uptake of alcohol use, a reduction in average alcohol consumption, a reduction in frequency of binge drinking, and a reduction in alcohol related harms. Trial registration This trial is registered with the Australian and New Zealand Clinical Trials registry, ACTRN12612000026820.