Heart failure (HF) is a chronic medical condition rapidly growing in prevalence. Evidence links HF to cognitive decline, obesity, and psychological distress. The current study examined the association between cognitive function and ejection fraction (EF%), anxiety, depression, and obesity in inpatient HF. Patients completed the Generalized Anxiety Disorder 7-Item Scale (GAD-7), Patient Health Questionnaire 9-Item Scale (PHQ-9), and Mini-Cog while hospitalized for HF. Additional demographic and medical information was gathered via chart review. All models controlled for age. Of 117 patients assessed (49% male), 55% (n = 64) were obese. ANCOVA analyses were conducted comparing those with obesity and without on cognitive function: model A included EF%, model B included depression, and model C included anxiety. All three models were significantly related to cognitive function. There was a significant interaction effect of EF% and obesity and of anxiety and obesity to predict Mini-Cog scores. Post hoc partial correlational analyses revealed that anxiety was negatively associated with Mini-Cog scores among only patients without obesity. Depression was not significantly related to cognitive function in either group. However, patients with obesity demonstrated higher depression and anxiety than patients without. Results suggest that at lower EF%, and with higher anxiety, patients without obesity may be at greater risk of cognitive dysfunction than those with obesity. Cognitive dysfunction among HF patients with obesity may be independent of psychological distress. These findings may reflect the "obesity paradox" observed among HF patients, in that patients with obesity may have a different biopsychosocial presentation, which may lead to unexpected clinical outcomes. Further research is necessary to articulate the relationship of obesity and cognitive function in HF.

A significant body of evidence suggests that poor dietary intake is associated with reduced cognitive function. However, few studies have examined this relation in poor urban settings. Our brief review suggests that (a) higher overall diet quality may play a particularly important role in cognitive function among the poorest; and (b) greater vitamin E intake is related to better cognitive performance, at least in part, via fewer depressive symptoms. The broader recent literature strongly suggests the beneficial role of diet for learning and memory, and potentially synergistic influences on other cognitive domains. However, adherence to healthful diet among urban poor may be limited by factors such as cost and access. Here, we propose several potential moderators and mediators of diet-cognition relations among urban poor. Future studies should focus on the complex interplay among factors that influence the role of diet in cognitive function among poor, urban-dwelling persons.

Evidence suggests social support may buffer brain pathology. However, neither its association with hippocampal volume, a marker of Alzheimer’s disease risk, nor the role of race in this association has been fully investigated. Multiple regression analyses examined relations of total social support to magnetic resonance imaging-assessed gray matter (GM) hippocampal volumes in the total sample ( n = 165; mean age = 68.48 year), and in race-stratified models of African American and White older adults, adjusting for select covariates. Results showed greater social support was associated with greater GM hippocampal volumes among African American older adults only ( p < .01). Our findings suggest greater total social support may play a role in supporting the hippocampus, particularly among African American older adults, who had lower hippocampal volumes than their White counterparts. Further research is needed to test these questions longitudinally and examine which aspects of social support may promote hippocampal integrity, specifically.

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Neighborhood disadvantage has been linked to poor health; however, research has not adequately examined its influence, across multiple domains of disadvantage, on neurocognitive function and underlying brain health in older adults. Thus, the objective was to examine associations between neighborhood disadvantage, brain health, and neurocognitive performance, and examine age and sex as effect modifiers. The analysis included 136 older adults with a mean age of 68.04y who underwent neuropsychological and psychosocial testing and 3T cranial magnetic resonance imaging. Neighborhood disadvantage was characterized using the Area Deprivation Index (ADI). Multivariable regression analysis, adjusted for age, sex, education, and depression, showed that greater ADI score (greater disadvantage) was associated with poorer working memory performance (p&lt;.05) and lower hippocampal volumes (p&lt;.05), with no evidence of effect modification. Results suggest that greater neighborhood disadvantage may play a role in working memory and brain structure, which are vital to quality of life in older adulthood.

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Poor sleep is common among older adults, and associated with hippocampal atrophy -- a strong predictor of memory decrements. Underlying this association are psychosocial risk factors, such as generalized anxiety, that may further exacerbate poor sleep and brain pathology. Given that poor sleep and generalized anxiety are often comorbid, there is a critical need to establish whether generalized anxiety is related to hippocampal volume among poor sleepers. To address this gap, this cross-sectional study examined the relationship between generalized anxiety (GAD-7), and total hippocampal volume, and whether it varied as a function of sleep quality (PSQI Total &lt; 5 good sleepers; PSQI Total ≥ 5 poor sleepers). Data were analyzed from 165 older adults (mean age = 68.48y, 33% male, 41% African American), free of major disease. Linear regression analysis, adjusting for sex, race, education and depression, showed a statistically significant Generalized Anxiety x Sleep interaction for hippocampal volume (p=.02). Further probing of this interaction revealed that among poor sleepers, greater generalized anxiety was associated with lesser hippocampal volume (p=.01). Findings suggest generalized anxiety may influence hippocampal volume in the context of poor sleep among older adults. As poor sleep is associated with age-related neurodegeneration, our findings suggest that improvements in sleep quality may reduce the impact of generalized anxiety on hippocampal volume in older adulthood. Future research should examine whether generalized anxiety mediates relations of sleep quality to specific memory outcomes.