BackgroundDepression and anxiety disorders in young people are a global health concern. Parents have an important role in reducing the risk of these disorders, but cost-effective, evidence-based interventions for parents that can be widely disseminated are lacking.ObjectiveThis study aimed to examine the postintervention effects of the Partners in Parenting (PiP) program on parenting risk and protective factors for adolescent depression and anxiety, and on adolescent depression and anxiety symptoms.MethodsA two-arm randomized controlled trial was conducted with 359 parent-adolescent dyads, recruited primarily through schools across Australia. Parents and adolescents were assessed at baseline and 3 months later (postintervention). Parents in the intervention condition received PiP, a tailored Web-based parenting intervention designed following Persuasive Systems Design (PSD) principles to target parenting factors associated with adolescents’ risk for depression and anxiety problems. PiP comprises a tailored feedback report highlighting each parent’s strengths and areas for improvement, followed by a set of interactive modules (up to nine) that is specifically recommended for the parent based on individually identified areas for improvement. Parents in the active-control condition received a standardized package of five Web-based factsheets about adolescent development and well-being. Parents in both conditions received a 5-min weekly call to encourage progress through their allocated program to completion. Both programs were delivered weekly via the trial website. The primary outcome measure at postintervention was parent-reported changes in parenting risk and protective factors, which were measured using the Parenting to Reduce Adolescent Depression and Anxiety Scale (PRADAS). Secondary outcome measures were the adolescent-report PRADAS, the parent- and child-report Short Mood and Feelings Questionnaire (depressive symptoms), and parent- and child-report Spence Children’s Anxiety Scale (anxiety symptoms).ResultsParents in the intervention condition completed a mean of 73.7% of their intended personalized PiP program. A total of 318 parents (88.6%, 318/359) and 308 adolescents (92.8%, 308/332) completed the postintervention assessment. Attrition was handled using mixed model of repeated measures analysis of variance. As hypothesized, we found a significant condition-by-time interaction on the PRADAS, with a medium effect size, Cohen d=0.57, 95% CI 0.34-0.79. No significant differences between conditions were found at postintervention on any of the secondary outcome measures, with adolescent depressive (parent-report only) and anxiety (both parent- and adolescent-report) symptoms decreasing significantly from baseline to postintervention in both conditions.ConclusionsThe fully automated PiP intervention showed promising short-term effects on parenting behaviors that are associated with adolescents’ risk for depression and anxiety. Long-term follow-up is required to ascertain whether these effects translate into red...
Burgeoning research suggests that parents can reduce the risk of anxiety and depression in their adolescents and that parental self‐efficacy (PSE) may be related to parental risk and protective factors for these disorders. As there are currently no measures available to assess PSE in relation to parenting behaviors that may reduce adolescent risk for depression and anxiety, we developed and validated a measure of PSE, the Parental Self‐Efficacy Scale (PSES). Using a sample of 359 parents and 332 adolescents (aged 12–15), the PSES was found to have high reliability, confirmatory factor analysis supported its validity, and most of the hypothesized relationships between the PSES and other measures of parenting practices and adolescent depressive and anxiety symptoms were supported.
White‐Sutton syndrome is a rare developmental disorder characterized by global developmental delay, intellectual disabilities (ID), and neurobehavioral abnormalities secondary to pathogenic pogo transposable element‐derived protein with zinc finger domain (POGZ) variants. The purpose of our study was to describe the neurocognitive phenotype of an unbiased national cohort of patients with identified POGZ pathogenic variants. This study is based on a French collaboration through the AnDDI‐Rares network, and includes 19 patients from 18 families with POGZ pathogenic variants. All clinical data and neuropsychological tests were collected from medical files. Among the 19 patients, 14 patients exhibited ID (six mild, five moderate and three severe). The five remaining patients had learning disabilities and shared a similar neurocognitive profile, including language difficulties, dysexecutive syndrome, attention disorders, slowness, and social difficulties. One patient evaluated for autism was found to have moderate autism spectrum disorder. This study reveals that the cognitive phenotype of patients with POGZ pathogenic variants can range from learning disabilities to severe ID. It highlights that pathogenic variations in the same genes can be reported in a large spectrum of neurocognitive profiles, and that children with learning disabilities could benefit from next generation sequencing techniques.
Megalencephaly‐CApillary malformation‐Polymicrogyria (MCAP) syndrome results from somatic mosaic gain‐of‐function variants in PIK3CA. Main features are macrocephaly, somatic overgrowth, cutaneous vascular malformations, connective tissue dysplasia, neurodevelopmental delay, and brain anomalies. The objectives of this study were to describe the clinical and radiological features of MCAP, to suggest relevant clinical endpoints applicable in future trials of targeted drug therapy. Based on a French collaboration, we collected clinical features of 33 patients (21 females, 12 males, median age of 9.9 years) with MCAP carrying mosaic PIK3CA pathogenic variants. MRI images were reviewed for 21 patients. The main clinical features reported were macrocephaly at birth (20/31), postnatal macrocephaly (31/32), body/facial asymmetry (21/33), cutaneous capillary malformations (naevus flammeus 28/33, cutis marmorata 17/33). Intellectual disability was present in 15 patients. Among the MRI images reviewed, the neuroimaging findings were megalencephaly (20/21), thickening of corpus callosum (16/21), Chiari malformation (12/21), ventriculomegaly/hydrocephaly (10/21), cerebral asymmetry (6/21) and polymicrogyria (2/21). This study confirms the main known clinical features that defines MCAP syndrome. Taking into account the phenotypic heterogeneity in MCAP patients, in the context of emerging clinical trials, we suggest that patients should be evaluated based on the main neurocognitive expression on each patient.
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