Mechanisms underlying the association between adverse childhood experiences and racial disparities in later-life cognition.

OBJECTIVE: Adverse childhood experiences (ACEs) may be a risk factor for later-life cognitive disorders such as dementia; however, few studies have investigated underlying mechanisms, such as cardiovascular health and depressive symptoms, in a health disparities framework. METHOD: 418 community-dwelling adults (50% nonHispanic Black, 50% nonHispanic White) aged 55+ from the Michigan Cognitive Aging Project retrospectively reported on nine ACEs. Baseline global cognition was a z-score composite of five factor scores from a comprehensive neuropsychological battery. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression Scale. Cardiovascular health was operationalized through systolic blood pressure. A mediation model controlling for sociodemographics, childhood health, and childhood socioeconomic status estimated indirect effects of ACEs on global cognition via depressive symptoms and blood pressure. Racial differences were probed via t-tests and stratified models. RESULTS: A negative indirect effect of ACEs on cognition was observed through depressive symptoms [ß = -.040, 95% CI (-.067, -.017)], but not blood pressure, for the whole sample. Black participants reported more ACEs (Cohen's d = .21), reported more depressive symptoms (Cohen's d = .35), higher blood pressure (Cohen's d = .41), and lower cognitive scores (Cohen's d = 1.35) compared to White participants. In stratified models, there was a negative indirect effect through depressive symptoms for Black participants [ß = -.074, 95% CI (-.128, -.029)] but not for White participants. CONCLUSIONS: These results highlight the need to consider racially patterned contextual factors across the life course. Such factors could exacerbate the negative impact of ACEs and related mental health consequences and contribute to racial disparities in cognitive aging.

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.

Social engagement and its links to cognition differ across non-Hispanic Black and White older adults.

OBJECTIVE: Racial inequalities in dementia have been linked to disparities in socioeconomic status, chronic diseases, and psychosocial stress. Less focus has been given to psychosocial protective factors. Previous studies suggest that social engagement promotes better cognitive aging, but few have examined whether social engagement or its associations with cognition vary across non-Hispanic Whites (NHW) and Blacks (NHB). METHOD: Participants included 465 adults (53% NHB) from the Michigan Cognitive Aging Project (Mage = 63.59 ± 3.15) who completed a comprehensive neuropsychological battery. Social engagement was operationalized as network size, frequency of social activity participation, and social support. Cognition was operationalized using factor scores corresponding to five domains: episodic memory, executive functioning, processing speed, language, and visuospatial functioning. Cross-sectional associations between social engagement and cognitive outcomes were examined using race-stratified regressions controlling for age, sex/gender, education, wealth, marital status, depressive symptoms, and chronic diseases. RESULTS: There were no racial differences in social network size or social support. NHB participants reported less social activity participation than NHW participants. Social activity participation was positively associated with memory in NHW, but not NHB. CONCLUSIONS: These findings may suggest a threshold effect whereby NHB older adults are less likely to participate in social activities at the level needed to yield cognitive benefits. Lower social activity participation among NHB may reflect structural barriers and/or cultural differences in patterns of social engagement. This study highlights the need to improve measurement of and access to culturally relevant social activities for NHB to combat racial inequalities in cognitive aging. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Depressive Symptoms, Leisure Activity Engagement, and Global Cognition in Non-Hispanic Black and White Older Adults.

OBJECTIVES: Prior research indicates that depressive symptoms disproportionately affect cognition in non-Hispanic Blacks relative to non-Hispanic Whites. Depressive symptoms have been linked to worse global cognition in older adulthood through lower leisure activity engagement, but less is known regarding the distinct types of activities that drive these associations and whether associations involving depressive symptoms, leisure activities, and cognition differ across racial groups. METHODS: This cross-sectional study used data from the Michigan Cognitive Aging Project (n = 453, 52.80% Black, Mage = 63.60 years). Principal components analysis identified 6 subtypes of leisure activities (cognitive, creative, community, physical, children, and games). Mediation models examined whether distinct leisure activity subtypes mediated the association between depressive symptoms and performance on a comprehensive neuropsychological battery and whether race moderated these associations. RESULTS: There were no racial differences in the level of depressive symptoms after adjusting for sociodemographic, socioeconomic, and health covariates. Only lower cognitive activity engagement mediated the negative association between depressive symptoms and global cognition. Multigroup models revealed that this indirect effect was only evident in Blacks, who showed a stronger negative association between depressive symptoms and cognitive activity engagement than Whites. After accounting for indirect effects, a direct effect of higher depressive symptoms on worse cognition remained and did not differ across racial groups. DISCUSSION: Depressive symptoms may disproportionately affect cognition among Blacks through a greater negative impact on engagement in cognitively stimulating activities that have been shown to promote cognitive reserve. Additional research is necessary to identify other mechanisms linking depressive symptoms and cognition.

Effects of Stress Exposure Versus Appraisal on Episodic Memory Trajectories: Evidence for Risk and Resilience Among Black Older Adults.

OBJECTIVES: Chronic stressors, experienced disproportionately by Black older adults, are a risk factor for memory impairment. Racially patterned stress exposure may contribute to higher rates of Alzheimer's disease and related dementias (ADRD) among Black older adults compared with Whites, but less is known about the role of stress appraisal. This study examined whether chronic stress exposure mediates racial disparities in memory and whether stress appraisal moderates these associations. METHODS: Participants included 16,924 older adults (Mage = 67.39, 21% Black) from the 2010 and 2012 waves of the Health and Retirement Study who completed measures of chronic stress exposure (health, financial, housing, relationships, and caregiving) and appraisal. Latent growth curves modeled longitudinal performance on a word list memory task over 6 years. RESULTS: Black older adults reported greater stress exposure than Whites, and greater stress exposure partially mediated Black-White disparities in initial memory (standardized indirect effect = -0.002, p = .009). However, Black older adults appraised stressors as less upsetting than Whites. While stress appraisal did not moderate links between stress exposure and memory, appraising stressors as less upsetting was independently associated with better initial memory. Thus, Black-White disparities in initial memory was partially offset by Black participants' appraisal of stressors as less upsetting (standardized indirect effect = 0.002, p = .016). DISCUSSION: Reducing chronic stress exposure may reduce racial disparities in ADRD risk. The counteractive effect of stress appraisal on Black-White disparities in episodic memory highlights resilience factors among Black older adults that should be characterized in future research to move beyond deficit models of ADRD inequality.