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Aim: To study the prevalence and patterns of problematic gaming and gambling during the COVID-19 pandemic and the association with psychiatric traits and major types of anxiety categories. Method: 1067 young adults participated in both wave 3 (2018) and wave 4 (2021) of the SALVe Cohort. Associations with psychiatric symptoms and anxiety were examined using logistic regression and Chi-square tests. Results: Problematic gaming decreased by 1.3 percentage points to 23.2% since the start of the pandemic, while problematic gambling increased by 0.9 percentage points to 6.5% in w4. Average time spent playing video games/day decreased from 2.2 h (w3) to 1.7 h (w4), while increases in gaming activity were associated with worsened feelings of loneliness (p = 0.002), depression (p < 0.001), and anxiety (p < 0.01) during the pandemic. Predictors for problematic gaming at w4 were previous problematic gaming and social anxiety (p = < 0.001 and 0.01, respectively). Moreover, previous problem gambling also predicted problem gambling at w4 p < 0.001. All anxiety categories were associated with both problematic gaming and gambling when adjusted for age and sex. However, after adjusting for depression and insomnia, social anxiety was associated with problematic gaming (p < 0.001), while panic was associated with problem gambling (p < 0.001). Conclusion: Overall, problematic gaming has decreased since the start of the pandemic, while problem gambling has increased. Worsened feelings of loneliness, depression, and anxiety during the pandemic are associated with increased gaming. Moreover, the association between problematic gaming and gambling and anxiety is independent of depression and sleep problems. [ABSTRACT FROM AUTHOR]

Many of the survivors of the novel coronavirus disease (COVID-19) are suffering from persistent symptoms, causing significant morbidity and decreasing their quality of life, termed "post-COVID-19 syndrome" or "long COVID". Understanding the mechanisms surrounding PCS is vital to developing the diagnosis, biomarkers, and possible treatments. Here, we describe the prevalence and manifestations of PCS, and similarities with previous SARS epidemics. Furthermore, we look at the molecular mechanisms behind the neurological features of PCS, where we highlight important neural mechanisms that may potentially be involved and pharmacologically targeted, such as glutamate reuptake in astrocytes, the role of NMDA receptors and transporters (EAAT2), ROS signaling, astrogliosis triggered by NF-κB signaling, KNDy neurons, and hypothalamic networks involving Kiss1 (a ligand for the G-protein-coupled receptor 54 (GPR54)), among others. We highlight the possible role of reactive gliosis following SARS-CoV-2 CNS injury, as well as the potential role of the hypothalamus network in PCS manifestations. [ABSTRACT FROM AUTHOR]