Internalizing and externalizing pathways to internet gaming disorder: the roles of anger and social anxiety

BackgroundInternet Gaming Disorder (IGD) represents a significant behavioral health concern, yet the roles of internalizing and externalizing psychological vulnerabilities in its development remain underexplored, particularly in Arabic-speaking populations.ObjectiveThis study examined anger and social anxiety as distinct externalizing and internalizing predictors of IGD severity in a Saudi Arabian community sample.MethodsA cross-sectional survey was administered to 303 participants (60.1% female; estimated mean age = 29.79 years, SD = 8.83) across five regions of Saudi Arabia. Participants completed the Internet Gaming Disorder Scale–Short Form (IGDS9-SF), a three-item Anger Screening Scale, and a two-item Social Anxiety screener. Hierarchical linear regression and structural equation modeling (SEM) were conducted to examine unique and incremental contributions of anger and social anxiety to IGD symptoms.ResultsAnger and social anxiety were strongly intercorrelated (r = .86, p <.001) but demonstrated divergent patterns in multivariate models. Hierarchical regression indicated that both predictors contributed unique variance when entered simultaneously, with anger positively and social anxiety negatively predicting IGD after controlling for shared variance. However, SEM clarified that only social anxiety significantly predicted latent IGD severity (β = .32, p = .027), whereas anger did not (β = .07, p = .68). The final model explained approximately 13% of variance in IGD symptoms.ConclusionsSocial anxiety was associated with IGD severity as a distinct internalizing correlate, consistent with avoidance-based coping and online social preference accounts. These preliminary, cross-sectional findings suggest that social anxiety warrants consideration in future IGD screening and research efforts in Arabic-speaking contexts.

Perception of social support and psychological well-being among mothers of individuals with intellectual disabilities: the mediating role of self-efficacy

BackgroundThe aim of this study is to examine the mediating role of self-efficacy in the relationship between social support perception and psychological well-being among mothers of individuals with intellectual disabilities.MethodsA correlational survey model was used in this study in line with the research objectives. The study group consisted of mothers of individuals with intellectual disabilities (n=80) in two central districts of Malatya province. Convenience sampling was employed in the study. The Psychological Well-being Scale was used to measure the psychological well-being of the participating mothers, the “Perceived Support Scale for Families of Children with Disabilities” was used to measure their perceived levels of social support, and the “Parental Self-Efficacy Scale” was used to measure their self-efficacy. In addition, a personal information form was used to introduce the socio-demographic characteristics of the participants. Descriptive statistics were calculated for the variables, and the normality assumption was examined using the Kolmogorov-Smirnov and Shapiro-Wilk tests. The relationships between the variables were evaluated using Pearson’s product-moment correlation analysis. Mediation analyses were performed using the PROCESS Macro (Model 4) developed by Hayes, and the significance of indirect effects was tested using the bootstrap method (5000 samples). The internal consistency reliability of the scales used in this study sample was assessed using Cronbach’s alpha coefficient.ResultsThere are positive and significant relationships between each of the perceived social support sub-dimensions of appreciation, informational, emotional, and companionship and self-efficacy (r = 0.28–0.36; p <0.05). A positive and significant relationship was also found between the total perceived social support score and self-efficacy (r = 0.37, p <0.01). In contrast, no direct significant relationships were found between perceived social support and its sub-dimensions and psychological well-being (p> 0.05). Psychological well-being showed only a moderate, positive and significant relationship with self-efficacy (r = 0.45, p <0.01).ConclusionsIn conclusion, it can be said that the relationship between perceived social support and psychological well-being is not direct, but indirect, mediated by self-efficacy.

From cats to cortex: T. gondii and psychosis, depression, and anxiety

This review examines whether cat ownership, via exposure to the neurotropic parasite T. gondii, contributes to vulnerability for psychotic, depressive, and anxiety symptoms. T. gondii establishes lifelong latent infection in the brain and muscle, where it can modulate dopaminergic signaling, neuroinflammation, and tryptophan–kynurenine metabolism, providing a biologically plausible pathway to altered cognition, mood, and behavior. Epidemiological and meta-analytic data indicate small-to-moderate associations between T. gondii seropositivity and schizophrenia, with more variable but suggestive links to depression and anxiety. Evidence for cat ownership as an independent risk factor is inconsistent: some cohorts and recent meta-analyses report elevated odds of schizophrenia-related outcomes in those exposed to cats, whereas rigorously controlled studies frequently find attenuated or null effects. Methodological limitations, alternative explanations, and cultural implications are discussed, and priorities for mechanism-informed, longitudinal and interventional research are outlined.

Extreme heat is worsening faster for Black Americans

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Good morning. After what sometimes felt like endless speculation, FDA Commissioner Marty Makary resigned from his role yesterday. Kyle Diamantas, the agency’s top food regulator, will step in as acting commissioner. STAT’s Lizzy Lawrence has the details. And Matt Herper has a hot take: Marty Makary was the worst FDA commissioner in 25 years.

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Gene Therapy ETX101 Improves Seizures and Neurodevelopment in Dravet Syndrome in Phase I/II

Dravet syndrome has long represented one of the most challenging pediatric epilepsies encountered in neurology and genetic medicine. Caused primarily by loss‑of‑function variants in SCN1A, the disorder emerges in infancy with prolonged febrile seizures and evolves into a lifelong condition marked by treatment‑resistant epilepsy, developmental delay, and significant morbidity. As the gene and cell therapy community gathers for the American Society of Gene and Cell Therapy (ASGCT) Annual Meeting, the field’s attention is turning toward approaches capable not only of reducing seizures but also of altering the developmental trajectory that defines the disorder. This year’s Presidential Symposium features new data on ETX101, an investigational gene regulation therapy from Encoded Therapeutics, that appears to move the needle on both fronts.

Encoded Therapeutics, a clinical‑stage biotechnology company developing precision genetic medicines for severe neurological disorders, has engineered ETX101 as a one‑time AAV9‑based therapy designed to increase expression of SCN1A. Rather than replacing or editing the gene, ETX101 aims to restore physiologic sodium channel function in inhibitory interneurons. The company’s Phase I/II POLARIS program is evaluating the therapy across multiple international sites in children ranging from six months to seven years of age.

The dataset presented at the ASGCT Presidential Symposium expands the emerging clinical profile of ETX101, incorporating additional patients, early readouts from the highest dose level, and longer‑term follow‑up. Across the cohort, treatment with a single intracerebroventricular dose produced a robust and dose‑dependent antiseizure effect that persisted through 52 weeks of observation. At dose level three, children experienced a median seizure reduction of approximately 76%, a notable finding given that this developmental window is typically associated with escalating seizure burden despite standard therapies. Early data from the top dose level suggest even stronger responses in participants who did not receive sirolimus, consistent with preclinical evidence that the drug can dampen protein expression.

Beyond seizure control, the therapy appears to influence developmental domains that are rarely improved in Dravet syndrome. Children who reached one year of follow‑up demonstrated measurable gains across communication, motor function, and other adaptive behaviors, as assessed by caregiver‑reported Vineland Adaptive Behavior Scales. Particularly striking were the trajectories of children treated before age two. In this group, cognitive assessments showed early and sustained divergence from the stagnation observed in the ENVISION natural history study, with trajectories more consistent with neurotypical development over the first year after treatment.

Families and clinicians have taken note of the dual signal emerging from the POLARIS dataset. “Parents of children with Dravet syndrome live with the fear of every seizure and the heartbreak of watching development stall,” said Mary Anne Meskis, CEO of the Dravet Syndrome Foundation. “To see the early and robust seizure reductions paired with meaningful developmental gains is profoundly encouraging. Families have been waiting for therapies that don’t just manage symptoms but give their children a chance to keep learning and growing.”

Encoded’s chief medical officer, Sal Rico, MD, PhD, underscored the significance of the findings. “Watching these young children not only achieve durable seizure reduction but also show early evidence of neurodevelopmental rescue is truly remarkable,” he said. “These data reinforce our belief that ETX101 has the potential to change the course of the disease and future outlook for the Dravet community.”

ETX101 has been well tolerated across all four dose levels, with no treatment‑related serious adverse events. Transaminase elevations, a known AAV class effect, were the most common treatment‑related finding; they were asymptomatic and resolved with standard management.

As the ASGCT community continues to explore the boundaries of genetic medicine, ETX101’s early results highlight the promise of targeted gene regulation as a therapeutic modality. For a disorder like Dravet syndrome, the possibility of addressing both seizures and developmental delay marks an important moment for the field.

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