Coping Styles and Cognitive Function in Older Non-Hispanic Black and White Adults.

OBJECTIVES: Coping styles refer to cognitive and behavioral patterns used to manage the demands of stressors, and effective coping represents a psychological resource. Some studies have linked coping styles to executive functioning, but less is known about coping styles and their associations with cognition across social groups known to differ in stress exposure and dementia risk. This study aimed to characterize associations between coping styles and cognitive functioning across non-Hispanic Black and non-Hispanic White older adults. METHODS: Participants were drawn from the Michigan Cognitive Aging Project (N = 453; age mean (SD) = 63.6 (3.2); 53% non-Hispanic Black). Problem-focused and emotion-focused coping were measured using the Coping Orientation to Problems Experienced Inventory. Global cognition was a composite of 5 cognitive domain scores derived from comprehensive neuropsychological tests. Cross-sectional associations between coping styles and cognition were examined using race-stratified regressions controlling for demographic and health covariates. RESULTS: Black older adults reported more emotion-focused coping than White older adults, but there were no race differences in problem-focused coping. Among Black older adults, less problem-focused coping and more emotion-focused coping were each associated with worse cognition. Among White older adults, emotion-focused coping was marginally linked to cognition. DISCUSSION: Greater emotion-focused coping among Black older adults may reflect greater exposure to stressors that are uncontrollable. Patterns of racial differences in coping-cognition links are in line with the social vulnerabilities hypothesis. Coping style may be a particularly important psychosocial resource for cognitive health among Black older adults that could be incorporated into culturally relevant interventions.

Links between early-life contextual factors and later-life cognition and the role of educational attainment.

OBJECTIVE: Educational attainment is a well-documented predictor of later-life cognition, but less is known about upstream contextual factors. This study aimed to identify which early-life contextual factors uniquely predict later-life global cognition and whether educational attainment mediates these relationships. METHOD: Participants were drawn from the Michigan Cognitive Aging Project (N = 485; Mage = 63.51; SDage = 3.13; 50% non-Hispanic Black). Early-life exposures included U.S. region of elementary school (Midwest, South, Northeast), average parental education, household composition (number of adults (1, 2, 3+), number of children), school racial demographics (predominantly White, predominantly Black, diverse), self-reported educational quality, and school type (public/private). Later-life global cognition was operationalized with a factor score derived from a comprehensive neuropsychological battery. Sequential mediation models controlling for sociodemographics estimated total, direct, and indirect effects of early-life contextual factors on cognition through educational attainment (years). RESULTS: Higher educational quality, higher parental education, and attending a private school were each associated with better cognition; attending a predominantly Black or diverse school and reporting three or more adults in the household were associated with lower cognition. After accounting for educational attainment, associations remained for educational quality, school type, and reporting three or more adults in the household. Indirect effects through educational attainment were observed for school region, educational quality, school racial demographics, and parental education. CONCLUSIONS: School factors appear to consistently predict later-life cognition more than household factors, highlighting the potential long-term benefits of school-level interventions for cognitive aging. Future research should consider additional mediators beyond educational attainment such as neighborhood resources and childhood adversity.

Longitudinal associations between racial discrimination and hippocampal and white matter hyperintensity volumes among older Black adults.

RATIONALE: Non-Hispanic Black older adults are at higher risk of Alzheimer's disease and related dementias (ADRD) than non-Hispanic Whites, which reflects racial disparities in both brain and cognitive health. Discrimination may contribute to these disparities, but much of the research on discrimination and ADRD outcomes is cross-sectional and/or does not disaggregate experiences of discrimination by attribution. Focusing specifically on racial discrimination and considering longitudinal brain outcomes may advance our understanding of the role of discrimination in explaining disproportionate rates of ADRD among non-Hispanic Black older adults. METHODS: In total, 221 non-Hispanic Black participants in the Washington Heights-Inwood Columbia Aging Project completed multiple measures of discrimination at one time point and structural magnetic resonance imaging (MRI) scans at two time points. Everyday discrimination and lifetime discrimination were operationalized first as aggregate experiences of discrimination (regardless of identity attributions) and then as racial discrimination per se. MRI outcomes included hippocampal and white matter hyperintensity (WMH) volumes. Latent difference score models estimated associations between the discrimination measures and each MRI outcome over four years. RESULTS: Aggregate discrimination (regardless of attributions) was not associated with either outcome. Lifetime racial discrimination was associated with lower initial hippocampal volume. Everyday racial discrimination was associated with faster accumulation of WMH over time. CONCLUSIONS: Racial discrimination may be detrimental for brain aging among non-Hispanic Black older adults, which may contribute to their disproportionate dementia burden. Disaggregating discrimination by attribution may clarify research on racial inequalities in brain and cognitive aging, as racial discrimination appears to be particularly toxic.

Associations between social network components and cognitive domains in older adults.

Previous research shows that social network components are associated with cognitive function later in life. However, fewer studies consider different cognitive domains or disaggregate the social network by relationship type. Using data from 2,553 participants aged 65 or older in the Health and Retirement Study's Harmonized Cognitive Assessment Protocol, this study examined relationships between social network structure (i.e., size, contact frequency) and quality (i.e., support, strain) and performance in five cognitive domains (i.e., episodic memory, executive function, visuoconstruction, language, and processing speed) 2-4 years later, controlling for sociodemographics and previous global cognition. Separate linear regressions were conducted for each cognitive outcome. When averaged across relationship types, network size was not associated with any domain. Contact frequency was positively associated with all domains except episodic memory. Support and strain were negatively associated with all cognitive domains. When considering individual relationship types, larger friend networks were positively associated with visuoconstruction, and greater contact frequency with friends was positively associated with all cognitive domains. Larger family networks were associated with worse executive function, visuoconstruction, and speed. Strain from friends had a negative relationship with every domain except episodic memory. Support from family was negatively associated with episodic memory, executive function, and language. These associations were equivalent to one to 3.5 years of cognitive aging. These results showed that both social network structure and quality may be consequential for cognitive functioning and that links between social relations and cognition differ across domains and as a function of relationship type. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

In vivo imaging of disturbed pre- and post-synaptic dopaminergic signaling via arachidonic acid in a rat model of Parkinson's disease.

BACKGROUND: Parkinson's disease involves loss of dopamine (DA)-producing neurons in the substantia nigra, associated with fewer pre-synaptic DA transporters (DATs) but more post-synaptic dopaminergic D2 receptors in terminal areas of these neurons. HYPOTHESIS: Arachidonic acid (AA) signaling via post-synaptic D2 receptors coupled to cytosolic phospholipase A2 (cPLA2) will be reduced in terminal areas ipsilateral to a chronic unilateral substantia nigra lesion in rats given D-amphetamine, which reverses the direction of the DAT, but will be increased in rats given quinpirole, a D2-receptor agonist. METHODS: D-amphetamine (5.0 mg/kg i.p.), quinpirole (1.0 mg/kg i.v.), or saline was administered to unanesthetized rats having a chronic unilateral lesion of the substantia nigra. AA incorporation coefficients, k* (radioactivity/integrated plasma radioactivity), markers of AA signaling, were measured using quantitative autoradiography in 62 bilateral brain regions following intravenous [1-(14)C]AA. RESULTS: In rats given saline (baseline), k* was elevated in 13 regions in the lesioned compared with intact hemisphere. Quinpirole increased k* in frontal cortical and basal ganglia regions bilaterally, more so in the lesioned than intact hemisphere. D-amphetamine increased k* bilaterally but less so in the lesioned hemisphere. CONCLUSIONS: Increased baseline elevations of k* and increased responsiveness to quinpirole in the lesioned hemisphere are consistent with their higher D2-receptor and cPLA2 activity levels, whereas reduced responsiveness to D-amphetamine is consistent with dropout of pre-synaptic elements containing the DAT. In vivo imaging of AA signaling using dopaminergic drugs can identify pre- and post-synaptic DA changes in animal models of Parkinson's disease.