This systematic review examines associations between parental socioeconomic disadvantage and childhood attention deficit/hyperactivity disorder (ADHD). Socioeconomic status (SES) was measured by parental income, education, occupation and marital status. Results were mixed by measure of SES with no one aspect being differentially related to ADHD. 42 studies were included in the review, of which 35 found a significant univariate association between socioeconomic disadvantage and ADHD. Meta-analyses of dimensions of SES and their association with ADHD indicate that children in families of low SES are on average 1.85-2.21 more likely to have ADHD than their peers in high SES families. In spite of substantial between-study heterogeneity, there is evidence for an association between socioeconomic disadvantage and risk of ADHD measured in different ways. This is likely mediated by factors linked to low SES such as parental mental health and maternal smoking during pregnancy.

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Although recent typologies of female sexual offenders have recognized the importance of having a co-offender, the clinical characteristics of solo and co-female sexual offenders remain poorly understood. The aim of this study was to compare solo (n = 20) and co- (n = 20) female sexual offenders on a variety of clinical characteristics. It was found that although solo and co-offenders reported similar developmental experiences and psychological dispositions, differences were found in environmental niche, offense preceding, and positive factors. Specifically, solo offenders demonstrated a greater presence of personal vulnerabilities including mental health and substance abuse difficulties. Co-offenders reported a greater presence of environmentally based factors, including a current partner who was a known sex offender and involvement with antisocial peers. It is suggested that these results have implications for understanding assessment and intervention needs for these groups of sexual offenders.

In rodents, insufficient adenosine produces behavioral and physiological symptoms consistent with several comorbidities of autism. In rodents and humans, stimuli postulated to increase adenosine can ameliorate these comorbidities. Because adenosine is a broad homeostatic regulator of cell function and nervous system activity, increasing adenosine’s influence might be a new therapeutic target for autism with multiple beneficial effects.