Non-Hispanic Black older adults experience a disproportionate burden of Alzheimer’s Disease and related dementias (ADRD) risk compared to non-Hispanic White older adults. It is necessary to identify mechanisms that may be contributing to inequities in cognitive aging. Psychosocial stressors that disproportionately affect Black adults (e.g., discrimination) have the potential to impact brain health through stress pathways. The brain’s white matter, which appears to be particularly important for ADRD risk among Black older adults, may be uniquely vulnerable to stress-related physiological dysfunction. To further understand whether and how discrimination can affect ADRD risk, this study aimed to examine associations between multiple forms of racial discrimination and white matter integrity, operationalized through diffusion tensor imaging.

Cross-sectional data were obtained from 190 non-Hispanic Black residents aged 65+ without dementia in northern Manhattan. Racial discrimination was self-reported using the Everyday Discrimination and Major Experiences of Lifetime Discrimination scales. Example items from the Everyday Discrimination Scale include: “You are treated with less respect than other people”; “You are called names or insulted.” Example items from the Major Experiences of Lifetime Discrimination Scale include: “At any time in your life, have you ever been unfairly fired from a job?”; “Have you ever been unfairly denied a bank loan?” Racial discrimination was operationalized as experiences attributed to “race” or “skin color.” White matter integrity was assessed using fractional anisotropy (FA) via diffusion tensor imaging. Multivariable regression models evaluated the unique effects of everyday and major experiences of lifetime racial discrimination on mean FA in the whole brain and specific regions. Initial models controlled for age, sex/gender, intracranial volume, and white matter hyperintensities. Subsequent models additionally controlled for socioeconomic and health factors to consider potential confounders or mediators of the relationship between discrimination and white matter integrity.

Major experiences of lifetime discrimination were negatively associated with mean FA within the left cingulum cingulate gyrus and the right inferior fronto-occipital fasciculus. These associations persisted when controlling for additional covariates (i.e., education, depression, and cardiovascular diseases). In contrast, major experiences of lifetime discrimination were positively associated with mean FA within the right superior longitudinal fasciculus (temporal part). This association was attenuated when controlling for additional covariates. Everyday racial discrimination was not associated with mean FA in any regions.

These results extend prior work linking racial discrimination to brain health and provide evidence for both risk and resilience among Black older adults. Major experiences of lifetime racial discrimination, a proxy for institutional racism, may have a stronger effect on white matter integrity than everyday racial discrimination, a proxy for interpersonal racism. Educational opportunities and cardiovascular risk factors may represent mediators between racial discrimination and white matter integrity. White matter integrity within specific brain regions may be a mechanism through which racially patterned social stressors contribute to racial disparities in ADRD. Future research should characterize within-group heterogeneity in order to identify factors that promote resilience among Black older adults.

Obstructive sleep apnea (OSA) may be a modifiable risk factor for late-life cognitive impairment. We previously demonstrated that non-Hispanic Black older adults are less likely to be diagnosed with OSA despite having equal or greater health risk for OSA compared to non-Hispanic White older adults, and this disparity in diagnosis was strongest among individuals with lower education. Here, we aimed to determine 1) whether there are racial differences in continuous positive airway pressure (CPAP) treatment, 2) how CPAP treatment may influence OSA-cognition associations, and 3) whether CPAP differentially influences OSA-cognition associations across racial groups.

Cross-sectional data were obtained from 424 socioeconomically diverse community-dwelling adults ages 55-83 (63.4±3.2 years, 41.7% male, 53.5% Black) from the Michigan Cognitive Aging Project. Physician-diagnosed OSA and current CPAP use were self-reported. Global cognition was operationalized as a composite of five factor scores derived from a comprehensive neuropsychological battery. Racial group differences were investigated with chi-square and Fisher’s exact tests with statistical significance set at the .05 level. Associations between OSA and cognition (adjusted for age, gender, race, and years of education) were investigated with linear regressions. Subsequent models isolated effects of uncontrolled OSA by excluding individuals using CPAP. Racial differences in OSA-cognition associations were investigated with race-stratified models.

Fewer Black participants (9.2%) reported diagnosed OSA compared to White participants (12.3%; x2 (1, N=424) =5.314, p=.021, cp=.112). In the whole sample, 47.3% of participants with diagnosed OSA reported CPAP use, and this proportion did not differ across race (x2 [1, N=86] =.048, p=.826). In the whole sample, OSA diagnosis was only associated with cognition when CPAP users were excluded (excluding CPAP users: ß=-.085, SE=.037, p=.024; including CPAP users: ß=-.067, SE=.036, p=.062). In race-stratified models, diagnosed OSA was only associated with cognition among Black participants, and this association was stronger when CPAP users were excluded (excluding CPAP users: ß=-.142, SE=.060, p=.018; including CPAP users: ß=-.126, SE=.058, p=.030). Diagnosed OSA was not associated with cognition among White participants, irrespective of whether CPAP users were included (excluding CPAP users: ß=-.084,SE=.068, p=.215; including CPAP users: ß=-.056, SE=.064, p=.378).

Our findings support CPAP treatment as a potential intervention to mitigate late-life cognitive impairment among those with OSA. Despite being less likely to receive a diagnosis of OSA, Black older adults were equally likely to engage in CPAP treatment as White older adults when diagnosed. The detrimental impact of OSA on cognition may be more salient among Black older adults, which may reflect racial disparities in cardiovascular risk and/or resources that promote cognitive reserve. However, CPAP appears to be an effective treatment to reduce OSA-related cognitive impairment for Black older adults, highlighting the critical importance of diagnosis and treatment in this group. Intervention efforts that abate racial inequalities in access to quality healthcare in order to facilitate acquisition of a formal OSA diagnosis and CPAP treatment may help to reduce preventable cognitive health disparities among older adults.

Higher education is strongly associated with better cognitive function in older adults. Previous research has also showed that positive psychosocial factors, such as selfefficacy and emotional and instrumental support, are beneficial for late-life cognition. There is prior evidence of a buffering effect of self-efficacy on the relationship between educational disadvantage and poor cognition in older adults, however it is not known if other psychosocial factors modify the schooling-cognition relationship. We hypothesized that higher levels of emotional and instrumental support will diminish the association between lower education and lower cognitive test scores among older adults.

553 older adults without dementia (42.1% non-Latinx Black, 32.2% non-Latinx White, 25.7% Latinx; 63.2% women; average age 74.4 (SD 4.3)) from the Washington Heights-Inwood Columbia Aging Project. Neuropsychological tests assessed four cognitive domains (language, memory, psychomotor processing speed, and visuospatial function). Self-reported emotional and instrumental support were assessed with measures from NIH Toolbox. Linear regression estimated interactions between education and the two support measures on cognition in models stratified by cognitive domain and racial and ethnic group. Covariates included age, sex/gender, and chronic health conditions (e.g. heart disease, stroke, cancer, etc.).

Education was associated with cognition across racial and ethnic groups. For every one year of schooling, the processing speed z-score composite was 0.33 higher among Latinx participants, 0.10 among non-Latinx Black participants, and 0.03 higher among non-Latinx White participants. The education-cognition relationship was generally similar across cognitive domains with larger effects in non-Latinx Black and Latinx participants than in White participants. Low education was associated with slower processing speed among Black participants with low emotional support (B = 0.224, 95% CI [0.014, 0.096]), but there was no association between low education and processing speed among Black older adults with high levels of emotional support (beta for interaction = -.142, 95% CI [-0.061, -0.001]). A similar pattern of results was observed for instrumental support (beta for interaction = -.207, 95% CI [-0.064, 0.010]). There were no interactions between support and education on other cognitive domains or among Latinx and White participants.

We found that higher levels of emotional and instrumental support attenuate the detrimental effect of educational disadvantages on processing speed in older Black adults. This may occur via benefits of social capital, which provides access to health resources and knowledge, increased social interaction, an emotional outlet allowing the ability to better cope with stress. Longitudinal analyses are needed to examine temporal patterns of associations. In addition, improving equitable access to high quality schools will improve later-life cognitive outcomes for future generations of older adults. However, for the growing number of Black older adults who will not experience the benefits of structural improvements in the education system, emotional and instrumental support may represent a modifiable psychosocial factor to reduce their disproportionate burden of cognitive morbidity.

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.

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.

A negative indirect effect of ACEs on cognition was observed through depressive symptoms [β = −.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 [β = −.074, 95% CI (−.128, −.029)] but not for White participants.

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.

Adverse childhood experiences (ACEs) have been associated with worse cognitive health in older adulthood. This study aimed to extend findings on the specificity, persistence, and pathways of associations between two ACEs and cognition by using a comprehensive neuropsychological battery and a time-lagged mediation design.

Participants were 3304 older adults in the Health and Retirement Study Harmonized Cognitive Assessment Protocol. Participants retrospectively reported whether they were exposed to parental substance abuse or experienced parental physical abuse before age 18. Factor scores derived from a battery of 13 neuropsychological tests indexed cognitive domains of episodic memory, executive functioning, processing speed, language, and visuospatial function. Structural equation models examined self-reported years of education and stroke as mediators, controlling for sociodemographics and childhood socioeconomic status.

Parental substance abuse in childhood was associated with worse later-life cognitive function across all domains, in part via pathways involving educational attainment and stroke. Parental physical abuse was associated with worse cognitive outcomes via stroke independent of education.

This national longitudinal study in the United States provides evidence for broad and persistent indirect associations between two ACEs and cognitive aging via differential pathways involving educational attainment and stroke. Future research should examine additional ACEs and mechanisms as well as moderators of these associations to better understand points of intervention.

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.

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).

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.

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.

This study compared the level of education and tests from multiple cognitive domains as proxies for cognitive reserve.

The participants were educationally, ethnically, and cognitively diverse older adults enrolled in a longitudinal aging study. We examined independent and interactive effects of education, baseline cognitive scores, and MRI measures of cortical gray matter change on longitudinal cognitive change.

Baseline episodic memory was related to cognitive decline independent of brain and demographic variables and moderated (weakened) the impact of gray matter change. Education moderated (strengthened) the gray matter change effect. Non-memory cognitive measures did not incrementally explain cognitive decline or moderate gray matter change effects.

Episodic memory showed strong construct validity as a measure of cognitive reserve. Education effects on cognitive decline were dependent upon the rate of atrophy, indicating education effectively measures cognitive reserve only when atrophy rate is low. Results indicate that episodic memory has clinical utility as a predictor of future cognitive decline and better represents the neural basis of cognitive reserve than other cognitive abilities or static proxies like education.

Stress is a risk factor for numerous negative health outcomes, including cognitive impairment in late-life. The negative association between stress and cognition may be mediated by depressive symptoms, which separate studies have identified as both a consequence of perceived stress and a risk factor for cognitive decline. Pathways linking perceived stress, depressive symptoms, and cognition may be moderated by sociodemographics and psychosocial resources. The goal of this cross-sectional study was to identify modifying factors and enhance understanding of the mechanisms underlying the stress–cognition association in a racially and ethnically diverse sample of older adults.

A linear regression estimated the association between perceived stress and episodic memory in 578 older adults (Mage = 74.58) in the Washington Heights-Inwood Columbia Aging Project. Subsequent models tested whether depressive symptoms mediated the stress–memory relationship and whether sociodemographics (gender, race, and ethnicity) or perceived control moderated these pathways.

Independent of sociodemographics and chronic diseases, greater perceived stress was associated with worse episodic memory. This relationship was mediated by more depressive symptoms. Higher perceived control buffered the association between stress and depressive symptoms. There was no significant moderation by gender, race, or ethnicity.

Depressive symptoms may play a role in the negative association between perceived stress and cognition among older adults; however, longitudinal analyses and studies using experimental designs are needed. Perceived control is a modifiable psychological resource that may offset the negative impact of stress.

Previous cross-sectional studies have documented associations between positive psychosocial factors, such as self-efficacy and emotional support, and late-life cognition. Further, the magnitudes of concurrent associations may differ across racial and ethnic groups that differ in Alzheimer’s disease risk. The goals of this longitudinal study were to characterize prospective associations between positive psychosocial factors and cognitive decline and explicitly test for differential impact across race and ethnicity.

578 older adults (42% non-Hispanic Black, 31% non-Hispanic White, and 28% Hispanic) in the Washington Heights-Inwood Columbia Aging Project completed cognitive and psychosocial measures from the NIH Toolbox and standard neuropsychological tests over 2.4 years. Latent difference scores were used to model associations between positive psychosocial factors and cognitive decline controlling for baseline cognition, sociodemographics, depressive symptoms, physical health, and other positive psychosocial factors. Multiple-group modeling was used to test interactions between the positive psychosocial factors and race/ethnicity.

Higher NIH Toolbox Friendship scores predicted less episodic memory decline. One standard deviation increase in friendship corresponded to 6 fewer years of memory aging. This association did not significantly differ across racial/ethnic groups.

This longitudinal study provides support for the potential importance of friendships for subsequent episodic memory trajectories among older adults from three ethnic groups. Further study into culturally informed interventions is needed to investigate whether and how friend networks may be targeted to promote cognitive health in late life.

Social engagement may be an important protective resource for cognitive aging. Some evidence suggests that time spent with friends may be more beneficial for cognition than time spent with family. Because maintaining friendships has been demonstrated to require more active maintenance and engagement in shared activities, activity engagement may be one underlying pathway that explains the distinct associations between contact frequency with friends versus family and cognition.

Using two waves of data from the national survey of Midlife in the United States (n = 3707, Mage = 55.80, 51% female at baseline), we examined longitudinal associations between contact frequency with friends and family, activity engagement (cognitive and physical activities), and cognition (episodic memory and executive functioning) to determine whether activity engagement mediates the relationship between contact frequency and cognition.

The longitudinal mediation model revealed that more frequent contact with friends, but not family, was associated with greater concurrent engagement in physical and cognitive activities, which were both associated with better episodic memory and executive functioning.

These findings suggest that time spent with friends may promote both cognitively and physically stimulating activities that could help to preserve not only these social relationships but also cognitive functioning.