Grand Challenges: Social Justice and the Need for Evidence-Based Sex Offender Registry Reform

Sex offender registries, though popular, bring with them enormous fiscal costs and unintended consequences for offenders and communities. Consistent with the Grand Challenges, social workers can play a role in advocating for sex offender management policies that are better informed by evidence and thus a better use of resources. Registry reform would also moderate the stigma resulting from the sex offender label, and reduce barriers to offender reintegration. First, a brief history of registration laws and the research around their effectiveness will be provided, followed by a rationale for needed improvements in sex offender management policy. Finally, evidence-based recommendations for reform will be offered. Such changes can result in improved public safety outcomes and social justice in our communities

You Learn What You Live: Prevalence of Childhood Adversity in the Lives of Juveniles Arrested for Sexual Offenses

Social workers often find themselves working with children or adolescents who have been victims of adverse childhood experiences (ACEs), including youths who have ended up in the juvenile justice system. Childhood trauma has been linked to negative health, mental health, and behavioral outcomes across the lifespan. The aim of this study was to examine the prevalence rates of child maltreatment and household dysfunction in the lives of juveniles who have been arrested for sexual offenses (JSO; n = 6,549). ACE prevalence rates for JSOs were compared by gender to juveniles arrested for other crimes, to adults arrested for sexual offenses, and to the general population. Youths in the delinquency system in Florida had much higher rates of high-ACE scores than the general population, indicating that they came from households where the accumulation and variety of early adversity is a salient feature in their lives. For those who have engaged in sexually abusive behavior, the existence of early maltreatment and family problems was prominent. Through a better understanding of the traumatic experiences of these youths, we can inform and enhance interventions designed to improve the functioning of sexually abusive juvenile clients and their families, and reduce risk of future recidivism

A Multiancestral Genome-Wide Exome Array Study of Alzheimer Disease, Frontotemporal Dementia, and Progressive Supranuclear Palsy

Importance Previous studies have indicated a heritable component of the etiology of neurodegenerative diseases such as Alzheimer disease (AD), frontotemporal dementia (FTD), and progressive supranuclear palsy (PSP). However, few have examined the contribution of low-frequency coding variants on a genome-wide level. Objective To identify low-frequency coding variants that affect susceptibility to AD, FTD, and PSP. Design, Setting, and Participants We used the Illumina HumanExome BeadChip array to genotype a large number of variants (most of which are low-frequency coding variants) in a cohort of patients with neurodegenerative disease (224 with AD, 168 with FTD, and 48 with PSP) and in 224 control individuals without dementia enrolled between 2005-2012 from multiple centers participating in the Genetic Investigation in Frontotemporal Dementia and Alzheimer’s Disease (GIFT) Study. An additional multiancestral replication cohort of 240 patients with AD and 240 controls without dementia was used to validate suggestive findings. Variant-level association testing and gene-based testing were performed. Main Outcomes and Measures Statistical association of genetic variants with clinical diagnosis of AD, FTD, and PSP. Results Genetic variants typed by the exome array explained 44%, 53%, and 57% of the total phenotypic variance of AD, FTD, and PSP, respectively. An association with the known AD gene ABCA7 was replicated in several ancestries (discovery P = .0049, European P = .041, African American P = .043, and Asian P = .027), suggesting that exonic variants within this gene modify AD susceptibility. In addition, 2 suggestive candidate genes, DYSF (P = 5.53 × 10−5) and PAXIP1 (P = 2.26 × 10−4), were highlighted in patients with AD and differentially expressed in AD brain. Corroborating evidence from other exome array studies and gene expression data points toward potential involvement of these genes in the pathogenesis of AD. Conclusions and Relevance Low-frequency coding variants with intermediate effect size may account for a significant fraction of the genetic susceptibility to AD and FTD. Furthermore, we found evidence that coding variants in the known susceptibility gene ABCA7, as well as candidate genes DYSF and PAXIP1, confer risk for AD