Racial and Ethnic Disparities in COVID-19-Related Stressor Exposure and Adverse Mental Health Outcomes Among Health Care Workers.

OBJECTIVE: Racial and ethnic disparities in exposure to COVID-19-related stressors, pandemic-related distress, and adverse mental health outcomes were assessed among health care workers in the Bronx, New York, during the first wave of the pandemic. METHODS: The authors analyzed survey data from 992 health care workers using adjusted logistic regression models to assess differential prevalence of outcomes by race/ethnicity and their interactions. RESULTS: Compared with their White colleagues, Latinx, Black, Asian, and multiracial/other health care workers reported significantly higher exposure to multiple COVID-19-related stressors: redeployment, fear of being sick, lack of autonomy at work, and inadequate access to personal protective equipment. Endorsing a greater number of COVID-19-related stressors was associated with pandemic-related distress in all groups and with adverse mental health outcomes in some groups; it was not related to hazardous alcohol use in any of the groups. These associations were not significantly different between racial and ethnic groups. Latinx health care workers had significantly higher probabilities of pandemic-related distress and posttraumatic stress than White colleagues. Despite greater exposure to COVID-19-related stressors, Black, Asian, and multiracial/other health care workers had the same, if not lower, prevalence of adverse mental health outcomes. Conversely, White health care workers had a higher adjusted prevalence of moderate to severe anxiety compared with Asian colleagues and greater hazardous alcohol use compared with all other groups. CONCLUSIONS: Health care workers from racial and ethnic minority groups reported increased exposure to COVID-19-related stressors, suggestive of structural racism in the health care workforce. These results underscore the need for increased support for health care workers and interventions aimed at mitigating disparities in vocational exposure to risk and stress.

Lack of Associations Between C-Reactive Protein and Mood and Anxiety Symptoms in Adolescents.

Introduction: Increased peripheral inflammation has been consistently documented in both adult and pediatric depression. However, elevated levels of C-reactive protein (CRP), a nonspecific biomarker for inflammation, have been primarily reported in adults; whether CRP plays a similar role in adolescent depression has not been conclusively established. In our prior work, we identified relationships between CRP and reward neurocircuitry in adolescents with psychiatric symptoms (N = 64) but not with depressive symptoms. Extending this work, we sought to examine CRP across the full range of mood and anxiety symptom severity in a larger, clinically diverse cohort of psychotropic medication-free adolescents and healthy controls (HCs). Methods: Subjects were adolescents (N = 127, age: 15.17 ± 2.19 years, 78 female) with psychiatric symptoms (n = 96, including previous cohort of 64) and HC (n = 31). All completed a semi-structured psychiatric evaluation and dimensional assessments for depression, anxiety, anhedonia, and suicidality. Group-comparison and correlation analyses utilized nonparametric statistics controlled for body mass index, sex, and age at pFWE < 0.05. Results: No group differences were identified in CRP levels between the clinical cohort and HCs. In addition, correlations between CRP and clinical symptomatology were not significant in either the whole sample or the psychiatric group. Conclusions: We found that, unlike in adults, CRP was not associated with depressive symptoms. This suggests that inflammation in pediatric depression is more narrowly delimited at the onset of psychiatric symptoms and may only become systemic with chronicity.

Correlates of C-reactive protein with neural reward circuitry in adolescents with psychiatric symptoms.

INTRODUCTION: Increased inflammation has been implicated in many psychiatric conditions across ages. We previously reported relationships between blood cytokine levels and anhedonia, the decreased capacity to experience pleasure, as well as with reward brain activation in adolescents with psychiatric symptoms. Here, we sought to extend this work in a larger cohort of adolescents with psychiatric symptoms and assess the relationships of C-Reactive Protein (CRP, inflammation biomarker) with clinical symptoms and reward-related brain activation. METHODS: Subjects were 64 psychotropic-medication-free adolescents with psychiatric symptoms (ages: 15.17 ± 2.10, 44 female). All had psychiatric evaluations and dimensional assessments for anxiety, depression, anhedonia, and suicidality. Neuroimaging included the Reward Flanker fMRI Task examining brain activation during reward anticipation, attainment and positive prediction error. Both whole-brain and ROI analyses focusing on reward circuitry were performed. All analyses were controlled for BMI, age, and sex at pFWE < 0.05. RESULTS: No relationships were identified between CRP and clinical symptom severity. CRP was positively associated with brain activation during reward attainment in regions of the visual and dorsal attention networks, as well as during positive prediction error in the cerebellum. In ROI analyses, CRP was negatively correlated with brain activation during reward anticipation in dorsal anterior cingulate cortex. When subject with high CRP was excluded, CRP was also positively correlated with positive predication error activation in nucleus accumbens. CONCLUSION: Despite lack of associations of CRP with clinical symptomatology, our fMRI findings suggest a relationship between inflammation and brain function early course of psychiatric conditions.

Grape-Derived Polyphenols Ameliorate Stress-Induced Depression by Regulating Synaptic Plasticity.

Major depressive disorder (MDD) is associated with stress-induced immune dysregulation and reduced brain-derived neurotrophic factor (BDNF) levels in sensitive brain regions associated with depression. Elevated levels of proinflammatory cytokines and reduced BDNF levels lead to impaired synaptic plasticity mechanisms that contribute to the pathophysiology of MDD. There is accumulating evidence that the administration of polyphenols at doses ranging from 5 to 180 mg/kg of body weight can normalize elevated levels of proinflammatory cytokines and abnormal levels of BDNF and, thus, restore impaired synaptic plasticity mechanisms that mediate depressive behavior in animal models of stress. This review will focus on the mechanisms by which grape-derived polyphenols normalize impaired synaptic plasticity and reduce depressive behavior in animal models of stress.

Neuroimmune nexus of depression and dementia: Shared mechanisms and therapeutic targets.

Dysfunctional immune activity is a physiological component of both Alzheimer's disease (AD) and major depressive disorder (MDD). The extent to which altered immune activity influences the development of their respective cognitive symptoms and neuropathologies remains under investigation. It is evident, however, that immune activity affects neuronal function and circuit integrity. In both disorders, alterations are present in similar immune networks and neuroendocrine signalling pathways, immune responses persist in overlapping neuroanatomical locations, and morphological and structural irregularities are noted in similar domains. Epidemiological studies have also linked the two disorders, and their genetic and environmental risk factors intersect along immune-activating pathways and can be synonymous with one another. While each of these disorders individually contains a large degree of heterogeneity, their shared immunological components may link distinct phenotypes within each disorder. This review will therefore highlight the shared immune pathways of AD and MDD, their overlapping neuroanatomical features, and previously applied, as well as novel, approaches to pharmacologically manipulate immune pathways, in each neurological condition. LINKED ARTICLES: This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc.