The Psychological, Academic, and Economic Impact of COVID-19 on College Students in the Epicenter of the Pandemic.

Initial research has indicated that college students have experienced numerous stressors as a result of the pandemic. The current investigation enrolled the largest and most diverse sample of college students to date (N = 4714) from universities in New York (NY) and New Jersey (NJ), the epicenter of the North American pandemic in Spring 2020. We described the impact on the psychological, academic, and financial health of college students who were initially most affected and examined racial/ethnic group differences. Results indicated that students' mental health was severely affected and that students of color were disproportionately affected by academic, financial, and COVID-related stressors. Worry about COVID-19 infection, stressful living conditions, lower grades, and loneliness emerged as correlates of deteriorating mental health. COVID-19's mental health impact on college students is alarming and highlights the need for public health interventions at the university level.

Influences on childhood depressive symptoms: The effects of trauma and distress tolerance across age and sex groups.

BACKGROUND: Depression affects many children and adolescents, leading to poor academic performance, impaired psychosocial functioning, and an increased frequency of suicidal behavior. Depression has also been notably associated with trauma and distress tolerance. Our study sought to understand the relationships of these variables across age and sex categories in youth and adolescents. METHODS: The current study examined data from a total of 324 participants between the ages of 7 and 17 years-old who were a part of a larger study. Data related to age, sex, depression, trauma, and distress tolerance were examined. RESULTS: A multiple regression revealed a significant interaction between age and sex on depression severity. Further, trauma and age by sex categories significantly predicted depression score, as well as distress tolerance predicting depression score. Lastly, a regression analysis, including trauma, distress tolerance, and age by sex categories were significant predictors of depression. LIMITATIONS: The results are limited by the cross-sectional design. CONCLUSION: Clinicians should consider age by sex effects when treating childhood depression. Future research should further the understanding of depression across age and sex groups, as well as among children with extensive trauma experiences. Future research should also seek to further understand the implications of distress tolerance therapy on childhood depression.

Simultaneous EEG and pupillary evidence for post-error arousal during a speeded performance task.

Arousal evoked by detecting a performance error may provide a mechanism by which error detection leads to either adaptive or maladaptive changes in attention and performance. By pairing EEG data acquisition with simultaneous measurements of pupil diameter, which is thought to reflect norepinephrinergic arousal, this study tested whether transient changes in EEG oscillations in the alpha frequency range (8-12 Hz) following performance mistakes may reflect error-evoked arousal. In the inter-trial interval following performance mistakes (approximately 8% of trials), pupil diameter increased and EEG alpha power decreased, compared to the inter-trial interval following correct responses. Moreover when trials were binned based on pupil diameter on a within-subjects basis, trials with greater pupil diameter were associated with lower EEG alpha power during the inter-trial interval. This pattern of association suggests that error-related alpha suppression, like pupil dilation, reflects arousal in response to error commission. Errors were also followed by worse next-trial performance, implying that error-evoked arousal may not always be beneficial for adaptive control.

Grant Report on d-Serine Augmentation of Neuroplasticity-Based Auditory Learning in Schizophrenia †.

We report on the rationale and design of an ongoing NIMH sponsored R61-R33 project in schizophrenia/schizoaffective disorder. This project studies augmenting the efficacy of auditory neuroplasticity cognitive remediation (AudRem) with d-serine, an N-methyl-d-aspartate-type glutamate receptor (NMDAR) glycine-site agonist. We operationalize improved (smaller) thresholds in pitch (frequency) between successive auditory stimuli after AudRem as improved plasticity, and mismatch negativity (MMN) and auditory θ as measures of functional target engagement of both NMDAR agonism and plasticity. Previous studies showed that AudRem alone produces significant, but small cognitive improvements, while d-serine alone improves symptoms and MMN. However, the strongest results for plasticity outcomes (improved pitch thresholds, auditory MMN and θ) were found when combining d-serine and AudRem. AudRem improvements correlated with reading and other auditory cognitive tasks, suggesting plasticity improvements are predictive of functionally relevant outcomes. While d-serine appears to be efficacious for acute AudRem enhancement, the optimal dose remains an open question, as does the ability of combined d-serine + AudRem to produce sustained improvement. In the ongoing R61, 45 schizophrenia patients will be randomized to receive three placebo-controlled, double-blind d-serine + AudRem sessions across three separate 15 subject dose cohorts (80/100/120 mg/kg). Successful completion of the R61 is defined by ≥moderate effect size changes in target engagement and correlation with function, without safety issues. During the three-year R33, we will assess the sustained effects of d-serine + AudRem. In addition to testing a potentially viable treatment, this project will develop a methodology to assess the efficacy of novel NMDAR modulators, using d-serine as a "gold-standard".

Neural Predictors of the Antidepressant Placebo Response.

The antidepressant placebo response remains a barrier to the development of novel therapies for depression, despite decades of efforts to identify and methodologically address its clinical correlates. This manuscript reviews recent neuroimaging studies that aim to identify the neural signature of antidepressant placebo response. Data captured in clinical trials have primarily focused on antidepressant efficacy or predicting antidepressant response and have reliably implicated the rostral anterior cingulate cortex (rACC) in antidepressant placebo response, but also in medication response. Imaging and electroencephalography (EEG) experiments specifically interrogating the mechanism of antidepressant placebo response, while few, suggest the reward network, including opiate neurotransmission, is also involved. Therefore, while the rACC is likely involved in the antidepressant placebo response, its observation in isolation is unlikely to prospectively distinguish antidepressant placebo from medication responders. Instead, future studies of antidepressant placebo response should probe the reward network as a whole and incorporate sophisticated computational analytical approaches.