Identifying Moderators Of Response To The Penn Resiliency Program: A Synthesis Study

To identify moderators of a cognitive-behavioral depression prevention program’s effect on depressive symptoms among youth in early adolescence, data from three randomized controlled trials of the Penn Resiliency Program (PRP) were aggregated to maximize statistical power and sample diversity (N = 1145). Depressive symptoms, measured with the Children’s Depression Inventory (CDI; Kovacs 1992), were assessed at six common time points over two-years of follow-up. Latent growth curve models evaluated whether PRP and control conditions differed in the rate of change in CDI and whether youth- and family-level characteristics moderated intervention effects. Model-based recursive partitioning was used as a supplementary analysis for identifying moderators. There was a three-way interaction of PRP, initial symptom severity, and intervention site on growth in depressive symptoms. There was considerable variability in PRP’s effects, with the nature of the interaction between PRP and initial symptom levels differing considerably across sites. PRP reduced depressive symptoms among youth with unmarried parents, but not among those with married parents. Finally, PRP’s effects differed across school grade levels. Although initial symptom severity moderated PRP’s effect on depressive symptoms, it was not a reliable indicator of how well the intervention performed, limiting its utility as a prescriptive variable. Our primary analyses suggest that PRP’s effects are limited to youth whose parents are unmarried. The small number of fifth grade students (n = 25; 2 %) showed a delayed and sustained intervention response. Our findings underscore the importance of evaluating site, family, and contextual characteristics as moderators in future studies

Evaluating the Effectiveness of a School-Based Cognitive Behavioral Youth Depression Prevention Program in Improving Life Satisfaction

Depression is the leading cause of disability worldwide, known as the global burden of disease. Incident cases from 1990 to 2017 have increased by 49.86%. Additionally, rates have been seen to dramatically rise in adolescents aged 18-25 (17%) compared to rates in individuals aged 10-14 (1.1%). This makes it beneficial to have prevention programs for middle school aged children. The Penn Resiliency Program (PRP) is a youth depression prevention program focused on cultivating healthy thinking styles and behavioral coping skills. In our study, we used archival data from a randomized control trial of PRP to evaluate whether the program led to improvements in life satisfaction in adolescents. Life satisfaction was reported using the Satisfaction with Life Scale by Diener. We used mixed effects modeling to evaluate the data collected from the PRP clinical trial. It was found that children in PRP tended to report slightly higher levels of life satisfaction, but these differences were not statistically significant. We did not find compelling evidence that children in PRP reported higher life satisfaction levels than those who received no intervention. Residual diagnostic analyses showed minor departures from normality in our residuals at high and low ends of the distribution, but overall the statistical model assumptions appeared to be reasonable. In conclusion, the data does not show enough evidence to conclude that life satisfaction was improved. Future research should look at functional outcomes, e.g., the child’s academic and social wellbeing

A Meta-Analytic Review Of The Penn Resiliency Program\u27s Effect On Depressive Symptoms

The purpose of this review was to evaluate whether the Penn Resiliency Program (PRP), a group cognitive–behavioral intervention, is effective in targeting depressive symptoms in youths. We identified 17 controlled evaluations of PRP (N = 2,498) in which depressive symptoms had been measured via an online search of PsycINFO, Medline, ERIC, and ProQuest Dissertations and Theses and by requesting data from PRP researchers. We combined effect sizes (ESs; Glass’s d), using random effects models at postintervention and two follow-up assessments (6–8 and 12 months postintervention). PRP participants reported fewer depressive symptoms at postintervention and both follow-up assessments compared with youths receiving no intervention, with ESs ranging from 0.11 to 0.21. Subgroup analyses showed that PRP’s effects were significant at 1 or more follow-up assessments among studies with both targeted and universal approaches, when group leaders were research team members and community providers, among participants with both low and elevated baseline symptoms, and among boys and girls. Limited data showed no evidence that PRP is superior to active control conditions. Preliminary analyses suggested that PRP’s effects on depressive disorders may be smaller than those reported in a larger meta-analysis of depression prevention programs for older adolescents and adults. We found evidence that PRP significantly reduces depressive symptoms through at least 1-year postintervention. Future PRP research should examine whether PRP’s effects on depressive symptoms lead to clinically meaningful benefits for its participants, whether the program is cost-effective, whether CB skills mediate program effects, and whether PRP is effective when delivered under real-world conditions. (PsycINFO Database Record (c) 2013 APA, all rights reserved)(journal abstract

Depressive and anxiety symptom trajectories from school age through young adulthood in samples with autism spectrum disorder and developmental delay.

OBJECTIVE: The objectives of this study were to model growth in anxiety and depressive symptoms from late school age through young adulthood in individuals with autism spectrum disorder (ASD) and controls with developmental delay (DD), and to assess relationships among internalizing growth patterns, participant characteristics, baseline predictors, and distal outcomes. METHOD: Data were collected between ages 6 and 24 years in 165 participants (n = 109 with ASD; n = 56 with nonspectrum DD), most of whom received diagnostic evaluations in both childhood and early adulthood. Questionnaires were collected approximately every 3 to 6 months between ages 9 and 24 years. Parent-rated Child Behavior Checklist (CBCL), Adult Behavior Checklist (ABCL), and Developmental Behaviour Checklist anxiety- and depression-related subscale distributions were modeled with mixed-effects Poisson models, covarying diagnosis, age, verbal IQ (VIQ), gender, and significant 2- and 3-way interactions. RESULTS: Anxiety was positively associated with VIQ, and controlling for VIQ, both anxiety and depressive symptoms were greater in ASD than nonspectrum participants. Female gender predicted greater increases over time in anxiety and depressive symptoms for both diagnostic groups. Lower maternal education was associated with increasing internalizing symptoms in a subset of less verbal individuals with ASD. In exploratory post hoc analyses, internalizing symptoms were associated with poorer emotional regulation in school age, and with lower life satisfaction and greater social difficulties in early adulthood. CONCLUSION: Findings support previous claims that individuals with ASD are at particular risk for affect- and anxiety-specific problems. Although symptom levels in females increase at a faster rate throughout adolescence, males with ASD appear to have elevated levels of depressive symptoms in school age that are maintained into young adulthood

Social Support Seeking And Early Adolescent Depression And Anxiety Symptoms: The Moderating Role Of Rumination

This study examined how social support seeking and rumination interacted to predict depression and anxiety symptoms 6 months later in early adolescents (N = 118; 11-14 years at baseline). We expected social support seeking would be more helpful for adolescents engaging in low rather than high levels of rumination. Adolescents self-reported on all measures at baseline, and on depression and anxiety symptoms 6 months later. Social support seeking predicted fewer symptoms of depression and anxiety at low rumination levels but was not associated with benefits as rumination increased. For depression symptoms, social support seeking predicted more symptoms at high rumination levels. Results were stronger for emotion-focused than problem-focused support seeking and for depression compared with anxiety symptoms. These findings suggest that cognitive risk factors like rumination may explain some inconsistencies in previous social support literature, and highlight the importance of a nuanced approach to studying social support seeking

The immediate early gene Egr3 Is required for hippocampal induction of Bdnf by electroconvulsive stimulation

Early growth response 3 (Egr3) is an immediate early gene (IEG) that is regulated downstream of a cascade of genes associated with risk for psychiatric disorders, and dysfunction of Egr3 itself has been implicated in schizophrenia, bipolar disorder, and depression. As an activity-dependent transcription factor, EGR3 is poised to regulate the neuronal expression of target genes in response to environmental events. In the current study, we sought to identify a downstream target of EGR3 with the goal of further elucidating genes in this biological pathway relevant for psychiatric illness risk. We used electroconvulsive stimulation (ECS) to induce high-level expression of IEGs in the brain, and conducted expression microarray to identify genes differentially regulated in the hippocampus of Egr3-deficient (-/-) mice compared to their wildtype (WT) littermates. Our results replicated previous work showing that ECS induces high-level expression of the brain-derived neurotrophic factor (Bdnf) in the hippocampus of WT mice. However, we found that this induction is absent in Egr3-/- mice. Quantitative real-time PCR (qRT-PCR) validated the microarray results (performed in males) and replicated the findings in two separate cohorts of female mice. Follow-up studies of activity-dependent Bdnf exons demonstrated that ECS-induced expression of both exons IV and VI requires Egr3. In situ hybridization demonstrated high-level cellular expression of Bdnf in the hippocampal dentate gyrus following ECS in WT, but not Egr3-/-, mice. Bdnf promoter analysis revealed eight putative EGR3 binding sites in the Bdnf promoter, suggesting a mechanism through which EGR3 may directly regulate Bdnf gene expression. These findings do not appear to result from a defect in the development of hippocampal neurons in Egr3-/- mice, as cell counts in tissue sections stained with anti-NeuN antibodies, a neuron-specific marker, did not differ between Egr3-/- and WT mice. In addition, Sholl analysis and counts of dendritic spines in golgi-stained hippocampal sections revealed no difference in dendritic morphology or synaptic spine density in Egr3-/-, compared to WT, mice. These findings indicate that Egr3 is required for ECS-induced expression of Bdnf in the hippocampus and suggest that Bdnf may be a downstream gene in our previously identified biologically pathway for psychiatric illness susceptibility.US National Institute of Mental Health [R01MH097803, R21MH113154]; Natural Sciences and Engineering Research Council of CanadaOpen access journal.This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Positive allosteric modulation as a potential therapeutic strategy in anti-NMDA receptor encephalitis

N-methyl-d-aspartate receptors (NMDARs) are ionotropic glutamate receptors important for synaptic plasticity, memory, and neuropsychiatric health. NMDAR hypofunction contributes to multiple disorders, including anti-NMDAR encephalitis (NMDARE), an autoimmune disease of the CNS associated with GluN1 antibody-mediated NMDAR internalization. Here we characterize the functional/pharmacological consequences of exposure to CSF from female human NMDARE patients on NMDAR function, and we characterize the effects of intervention with recently described positive allosteric modulators (PAMs) of NMDARs. Incubation (48 h) of rat hippocampal neurons of both sexes in confirmed NMDARE patient CSF, but not control CSF, attenuated NMDA-induced current. Residual NMDAR function was characterized by lack of change in channel open probability, indiscriminate loss of synaptic and extrasynaptic NMDARs, and indiscriminate loss of GluN2B-containing and GluN2B-lacking NMDARs. NMDARs tagged with N-terminal pHluorin fluorescence demonstrated loss of surface receptors. Thus, function of residual NMDARs following CSF exposure was indistinguishable from baseline, and deficits appear wholly accounted for by receptor loss. Coapplication of CSF and PAMs of NMDARs (SGE-301 or SGE-550, oxysterol-mimetic) for 24 h restored NMDAR function following 24 h incubation in patient CSF. Curiously, restoration of NMDAR function was observed despite washout of PAMs before electrophysiological recordings. Subsequent experiments suggested that residual allosteric potentiation of NMDAR function explained the persistent rescue. Further studies of the pathogenesis of NMDARE and intervention with PAMs may inform new treatments for NMDARE and other disorders associated with NMDAR hypofunction.SIGNIFICANCE STATEMENTAnti-N-methyl-d-aspartate receptor encephalitis (NMDARE) is increasingly recognized as an important cause of sudden-onset psychosis and other neuropsychiatric symptoms. Current treatment leaves unmet medical need. Here we demonstrate cellular evidence that newly identified positive allosteric modulators of NMDAR function may be a viable therapeutic strategy.</jats:p

Parent Predictors Of Adolescents’ Explanatory Style

The current study tested the prospective relations (6-month lag) between three aspects of the parent-child relationship at Time 1 (T1) and adolescents’ explanatory styles at Time 2 (T2): caregiving behaviors, parents’ explanatory style for their own negative events, and parents’ explanatory style for their children’s negative events. The sample included 129 adolescents aged 11 to 14 years at baseline and their parents. Adolescents reported on their own explanatory style and their parents’ caregiving behaviors; parents self-reported on their caregiving behaviors and their explanatory style for their own and their children’s events. Regression analyses identified maternal acceptance as a significant predictor of T2 adolescents’ explanatory style. Marginal effects emerged for fathers’ psychological control and fathers’ explanatory style for their children’s events. Findings suggest that the ways parents—especially mothers—interact with their children may play a role in adolescents’ cognitive vulnerability to depression

Resilience Education

As a primary learning and social environment for most children, schools have tremendous potential to, and responsibility for, promoting resilience and well-being in children. This chapter reviews the rationale for focusing on resilience in education and illustrates some of the ways that schools can promote resilience in young people. Although resilience education can also encompass academic or educational resilience, the authors focus primarily on the power of schools to promote students’ social and emotional well-being and provide examples from their team’s work on school-based resilience and positive psychology interventions. As they hope to show, resilience education holds great promise in promoting the well-being of all students