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Objectives: Cross-sectional and longitudinal evidence from largely non-Hispanic White cohorts suggests that positive psychosocial factors, particularly self-efficacy and social support, may protect against late-life cognitive decline. Identifying potentially protective factors in racial/ethnic minority elders is of high importance due to their increased risk of Alzheimer’s disease. The overall goal of this study was to characterize cross-sectional associations between positive psychosocial factors and cognitive domains among Black, Hispanic, and White older adults. Methods: A total of 548 older adults (41% Black, 28% Hispanic, 31% White) in the Washington Heights-Inwood Columbia Aging Project completed cognitive and psychosocial measures from the NIH Toolbox and standard neuropsychological tests. Multiple-group regressions were used to compare cross-sectional associations between positive psychosocial factors and cognition across racial/ethnic groups, independent of demographics, depressive symptoms, and physical health. Results: Positive associations between self-efficacy and language did not significantly differ across race/ethnicity, although the bivariate association between self-efficacy and language was not significant among Hispanics. Additional positive associations were observed for Whites and Blacks, but not Hispanics. Negative associations between emotional support and purpose in life and working memory were seen only in Hispanics. Conclusions: Results confirm and extend the link between self-efficacy and cognition in late life, particularly for White and Black older adults. Previous studies on positive psychosocial factors in cognitive aging may not be generalizable to Hispanics. Longitudinal follow-up is needed to determine whether negative relationships between certain psychosocial factors and cognition in Hispanics reflect reverse causation, threshold effects, and/or negative aspects of having a strong social network. (JINS, 2018, 24, 294–304)

Being married may protect late-life cognition. Less is known about living arrangement among unmarried adults and mechanisms such as brain health (BH) and cognitive reserve (CR) across race and ethnicity or sex/gender. The current study examines (1) associations between marital status, BH, and CR among diverse older adults and (2) whether one's living arrangement is linked to BH and CR among unmarried adults. Cross-sectional data come from the Washington Heights-Inwood Columbia Aging Project ( = 778, 41% Hispanic, 33% non-Hispanic Black, 25% non-Hispanic White; 64% women). Magnetic resonance imaging (MRI) markers of BH included cortical thickness in Alzheimer's disease signature regions and hippocampal, gray matter, and white matter hyperintensity volumes. CR was residual variance in an episodic memory composite after partialing out MRI markers. Exploratory analyses stratified by race and ethnicity and sex/gender and included potential mediators. Marital status was associated with CR, but not BH. Compared to married individuals, those who were previously married (i.e., divorced, widowed, and separated) had lower CR than their married counterparts in the full sample, among White and Hispanic subgroups, and among women. Never married women also had lower CR than married women. These findings were independent of age, education, physical health, and household income. Among never married individuals, living with others was negatively linked to BH. Marriage may protect late-life cognition via CR. Findings also highlight differential effects across race and ethnicity and sex/gender. Marital status could be considered when assessing the risk of cognitive impairment during routine screenings.

The progression of Alzheimer's disease and related dementias (ADRDs) from prodromal state to dementia syndrome prompts researchers to identify early markers of cognitive decline. One potential risk marker is subjective memory concerns (SMCs). Individuals with greater perceived stress often report more cognitive concerns. Moreover, increased social support is linked to lower perceived stressors. Our previous cross-sectional work with an ethnoracially diverse sample of older adults reveals a positive relationship between chronic stress and SMCs, adjusting for demographic factors. It remains unknown if chronic stress and social support are longitudinally associated with SMCs (at the between- and within-person levels), particularly among older Hispanic/Latin Americans, who are notably underrepresented in ADRD research. The present research aims to address these gaps. Data for 84 Mexican Americans (Age = 62±6.97; Education = 10±3.57) were collected across three waves (24-to-30-month intervals) via the Health and Aging Brain Study: Health Disparities (HABS-HD). Exclusion criteria included depression, stroke, Alzheimer's disease, and/or other dementia diagnoses. Participants self-reported subjective memory concerns, chronic stress, and social support levels. Multilevel models were conducted to explore longitudinal associations between chronic stress and social support on SMCs, controlling for age, gender, and education. Findings showed significant between-subject effects of chronic stress (β = .15, p = .018, 95% CI [.03, .27]) and of social support (β = -.26, p < .001, 95% CI [-.40, -.12]) on SMCs. There were no significant within-person effects of chronic stress (β = .046, p = .122, 95% CI [-.012, .10]) or social support (β = -.045, p = .098, 95% CI [-.11, .0093]) on SMCs. Individuals with higher chronic stress and lower social support tended to report more memory concerns compared to individuals with lower chronic stress and higher social support. These findings suggest that Mexican Americans facing stressors or having fewer social supports may be a group particularly at risk for ADRDs. Future research may examine if social support mediates the between-person effects of long-term stressors on SMCs through a longitudinal mediation model.

Background The progression of Alzheimer’s disease and related dementias (ADRDs) from prodromal state to dementia syndrome prompts researchers to identify early markers of cognitive decline. One potential risk marker is subjective memory concerns (SMCs). Individuals with greater perceived stress often report more cognitive concerns. Moreover, increased social support is linked to lower perceived stressors. Our previous cross‐sectional work with an ethnoracially diverse sample of older adults reveals a positive relationship between chronic stress and SMCs, adjusting for demographic factors. It remains unknown if chronic stress and social support are longitudinally associated with SMCs (at the between‐ and within‐person levels), particularly among older Hispanic/Latin Americans, who are notably underrepresented in ADRD research. The present research aims to address these gaps. Method Data for 84 Mexican Americans (Age = 62±6.97; Education = 10±3.57) were collected across three waves (24‐to‐30‐month intervals) via the Health and Aging Brain Study: Health Disparities (HABS‐HD). Exclusion criteria included depression, stroke, Alzheimer’s disease, and/or other dementia diagnoses. Participants self‐reported subjective memory concerns, chronic stress, and social support levels. Multilevel models were conducted to explore longitudinal associations between chronic stress and social support on SMCs, controlling for age, gender, and education. Results Findings showed significant between‐subject effects of chronic stress (β = .15, p = .018, 95% CI [.03, .27]) and of social support (β = ‐.26, p < .001, 95% CI [‐.40, ‐.12]) on SMCs. There were no significant within‐person effects of chronic stress (β = .046, p = .122, 95% CI [‐.012, .10]) or social support (β = ‐.045, p = .098, 95% CI [‐.11, .0093]) on SMCs. Conclusions Individuals with higher chronic stress and lower social support tended to report more memory concerns compared to individuals with lower chronic stress and higher social support. These findings suggest that Mexican Americans facing stressors or having fewer social supports may be a group particularly at risk for ADRDs. Future research may examine if social support mediates the between‐person effects of long‐term stressors on SMCs through a longitudinal mediation model.

The Ad26.COV2.S vaccine 1 – 3 has demonstrated clinical efficacy against symptomatic COVID-19, including against the B.1.351 variant that is partially resistant to neutralizing antibodies 1 . However, the immunogenicity of this vaccine in humans against SARS-CoV-2 variants of concern remains unclear. Here we report humoral and cellular immune responses from 20 Ad26.COV2.S vaccinated individuals from the COV1001 phase I–IIa clinical trial 2 against the original SARS-CoV-2 strain WA1/2020 as well as against the B.1.1.7, CAL.20C, P.1 and B.1.351 variants of concern. Ad26.COV2.S induced median pseudovirus neutralizing antibody titres that were 5.0-fold and 3.3-fold lower against the B.1.351 and P.1 variants, respectively, as compared with WA1/2020 on day 71 after vaccination. Median binding antibody titres were 2.9-fold and 2.7-fold lower against the B.1.351 and P.1 variants, respectively, as compared with WA1/2020. Antibody-dependent cellular phagocytosis, complement deposition and natural killer cell activation responses were largely preserved against the B.1.351 variant. CD8 and CD4 T cell responses, including central and effector memory responses, were comparable among the WA1/2020, B.1.1.7, B.1.351, P.1 and CAL.20C variants. These data show that neutralizing antibody responses induced by Ad26.COV2.S were reduced against the B.1.351 and P.1 variants, but functional non-neutralizing antibody responses and T cell responses were largely preserved against SARS-CoV-2 variants. These findings have implications for vaccine protection against SARS-CoV-2 variants of concern. Analysis of the immunogenicity of the Ad26.COV2.S vaccine against the B1.351 and P.1 SARS-CoV-2 variants of concern shows reduced neutralization antibody titres, but comparable T cell responses and antibody-dependent effector functions.

The effective implementation of government policies and measures for controlling the coronavirus disease 2019 (COVID-19) pandemic requires compliance from the public. This study aimed to examine cross-sectional and longitudinal associations of trust in government regarding COVID-19 control with the adoption of recommended health behaviours and prosocial behaviours, and potential determinants of trust in government during the pandemic. This study analysed data from the PsyCorona Survey, an international project on COVID-19 that included 23 733 participants from 23 countries (representative in age and gender distributions by country) at baseline survey and 7785 participants who also completed follow-up surveys. Specification curve analysis was used to examine concurrent associations between trust in government and self-reported behaviours. We further used structural equation model to explore potential determinants of trust in government. Multilevel linear regressions were used to examine associations between baseline trust and longitudinal behavioural changes. Higher trust in government regarding COVID-19 control was significantly associated with higher adoption of health behaviours (handwashing, avoiding crowded space, self-quarantine) and prosocial behaviours in specification curve analyses (median standardised = 0.173 and 0.229, < 0.001). Government perceived as well organised, disseminating clear messages and knowledge on COVID-19, and perceived fairness were positively associated with trust in government (standardised = 0.358, 0.230, 0.056, and 0.249, < 0.01). Higher trust at baseline survey was significantly associated with lower rate of decline in health behaviours over time ( for interaction = 0.001). These results highlighted the importance of trust in government in the control of COVID-19.

To understand the roles of acute-phase viral dynamics and host immune responses in post-acute sequelae of SARS-CoV-2 infection (PASC), we enrolled 136 participants within 5 days of their first positive SARS-CoV-2 real-time PCR test. Participants self-collected up to 21 nasal specimens within the first 28 days post-symptom onset; interviewer-administered questionnaires and blood samples were collected at enrollment, days 9, 14, 21, 28, and month 4 and 8 post-symptom onset. Defining PASC as the presence of any COVID-associated symptom at their 4-month visit, we compared viral markers (quantity and duration of nasal viral RNA load, infectious viral load, and plasma N-antigen level) and host immune markers (IL-6, IL-10, TNF-α, IFN-α, IFN-γ, MCP, IP-10, and Spike IgG) over the acute period. Compared to those who fully recovered, those reporting PASC demonstrated significantly higher maximum levels of SARS-CoV-2 RNA and N-antigen, burden of RNA and infectious viral shedding, and lower Spike-specific IgG levels within 9 days post-illness onset. No significant differences were identified among a panel of host immune markers. Our results suggest early viral dynamics and the associated host immune responses play a role in the pathogenesis of PASC, highlighting the importance of understanding early biological markers in the natural history of PASC. Biological determinants for developing post-acute sequelae of SARS-CoV-2 infection are largely unclear. Here, by comparing markers during acute infection in individuals who developed PASC with those who recovered, the authors found that early viral dynamics and immune responses might play a role in PASC pathogenesis.

The pancreatic islet is a complex micro-organ containing numerous cell types, including endocrine, immune, and endothelial cells. The communication of these systems is lost upon isolation of the islets, and therefore the pathogenesis of diabetes can only be fully understood by studying this organized, multicellular environment in vivo . We have developed several adaptable tools to create a versatile platform to interrogate β-cell function in vivo . Specifically, we developed β-cell-selective virally-encoded fluorescent protein biosensors that can be rapidly and easily introduced into any mouse. We then coupled the use of these biosensors with intravital microscopy, a powerful tool that can be used to collect cellular and subcellular data from living tissues. Together, these approaches allowed the observation of in vivo β-cell-specific ROS dynamics using the Grx1-roGFP2 biosensor and calcium signaling using the GcAMP6s biosensor. Next, we utilized abdominal imaging windows (AIW) to extend our in vivo observations beyond single-point terminal measurements to collect longitudinal physiological and biosensor data through repeated imaging of the same mice over time. This platform represents a significant advancement in our ability to study β-cell structure and signaling in vivo , and its portability for use in virtually any mouse model will enable meaningful studies of β-cell physiology in the endogenous islet niche.

Prevention of viral escape and increased coverage against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern require therapeutic monoclonal antibodies (mAbs) targeting multiple sites of vulnerability on the coronavirus spike glycoprotein. Here we identify several potent neutralizing antibodies directed against either the N-terminal domain (NTD) or the receptor-binding domain (RBD) of the spike protein. Administered in combinations, these mAbs provided low-dose protection against SARS-CoV-2 infection in the K18-human angiotensin-converting enzyme 2 mouse model, using both neutralization and Fc effector antibody functions. The RBD mAb WRAIR-2125, which targets residue F486 through a unique heavy-chain and light-chain pairing, demonstrated potent neutralizing activity against all major SARS-CoV-2 variants of concern. In combination with NTD and other RBD mAbs, WRAIR-2125 also prevented viral escape. These data demonstrate that NTD/RBD mAb combinations confer potent protection, likely leveraging complementary mechanisms of viral inactivation and clearance. Krebs and colleagues identify multiple mAbs that recognize either the RBD or the NTD of SARS-CoV-2 spike protein that have potent cross-neutralizing activities against variants of concern. Combinatorial mAb cocktails have complementary effects on viral neutralization and Fc effector functions and can protect against SARS-CoV-2 escape mutants.

An acute bout of exercise can improve endothelial function and insulin sensitivity when measured on the day following exercise. Our aim was to compare acute high-intensity continuous exercise (HICE) to high-intensity interval exercise (HIIE) on circulating endothelial microparticles (EMPs) and insulin sensitivity in overweight/obese men and women. Inactive males (BMI = 30 ± 3, 25 ± 6 yr, n = 6) and females (BMI = 28 ± 2, 21 ± 3 yr, n = 7) participated in three experimental trials in a randomized counterbalanced crossover design: 1) No exercise control (Control); 2) HICE (20 min cycling @ just above ventilatory threshold); 3) HIIE (10 X 1-min @ ∼ 90% peak aerobic power). Exercise conditions were matched for external work and diet was controlled post-exercise. Fasting blood samples were obtained ∼ 18 hr after each condition. CD62E(+) and CD31(+)/CD42b- EMPs were assessed by flow cytometry and insulin resistance (IR) was estimated by homeostasis model assessment (HOMA-IR). There was a significant sex X exercise interaction for CD62E(+) EMPs, CD31(+)/CD42b- EMPs, and HOMA-IR (all P < 0.05). In males, both HICE and HIIE reduced EMPs compared to Control (P ≤ 0.05). In females, HICE increased CD62E(+) EMPs (P < 0.05 vs. Control) whereas CD31(+)/CD42b- EMPs were unaltered by either exercise type. There was a significant increase in HOMA-IR in males but a decrease in females following HIIE compared to Control (P<0.05). Overweight/obese males and females appear to respond differently to acute bouts of high-intensity exercise. A single session of HICE and HIIE reduced circulating EMPs measured on the morning following exercise in males but in females CD62E(+) EMPs were increased following HICE. Next day HOMA-IR paradoxically increased in males but was reduced in females following HIIE. Future research is needed to investigate mechanisms responsible for potential differential responses between males and females.