INS NYC 2024 Program

Paper	Paper Session 04 Program Schedule 02/15/2024 11:45 am - 01:15 pm Room: West Side Ballroom - Salon 3 Paper Session 04: Cognitive Aging and Related Topics 1 Final Abstract #3 Is Systemic Inflammation a Mediator of Longitudinal Psychosocial Stress-Memory Associations in Black and White Older Adults? Emily Morris, University of Michigan, Ann Arbor, United States Ketlyne Sol, University of Michigan, Ann Arbor, United States Kiana Scambray, University of Michigan, Ann Arbor, United States Ji Hyun Lee, University of Michigan, Ann Arbor, United States Jordan Palms, University of Michigan, Ann Arbor, United States Laura Zahodne, University of Michigan, Ann Arbor, United States Category: Aging Keyword 1: chronic stress Keyword 2: minority issues Keyword 3: memory disorders Objective: Growing research has established that psychosocial stressors at the interpersonal, community, and societal levels are negatively associated with memory performance and partially explain Black-White memory disparities memory in older adulthood. However, little is known regarding specific pathways linking psychosocial stress with memory, particularly over time. Systemic inflammation, as measured by C-reactive protein (CRP), may be one relevant biophysiological pathway, given known associations between stress and inflammation, particularly among Black older adults. This study used a robust cross-lagged longitudinal mediation framework to identify whether systemic inflammation is a mechanism underlying multilevel psychosocial stress-memory associations, and whether associations differ across older Black and White adults. Participants and Methods: Participants included 15,382 adults (22% Black participants, 78% White participants) aged 51 and older from the 2010 and 2012 waves of the Health and Retirement Study (HRS). Participants completed measures of interpersonal (everyday discrimination), community (neighborhood physical disorder), and societal (subjective societal status) stress at baseline (Wave 1). Systemic inflammation was operationalized as the CRP concentration measured by a high-sensitivity assay of capillary blood collected at Wave 2, two years after Wave 1. A composite of immediate and delayed recall of a 10-item word list from Wave 3 was the outcome variable, measured four years after Wave 1. Cross-lagged mediation analyses examined whether Wave 2 CRP mediated associations between Wave 1 psychosocial stressors and Wave 3 memory, controlling for autoregressive pathways of CRP at Wave 1 and memory at Waves 1 and 2, covariates (age, sex, education, and wealth, measured at Wave 1), and study enrollment year. Race-stratified mediation models estimated associations in Black and White participants separately. Results: While higher Wave 2 CRP was associated with worse Wave 3 memory (B= -.024, SE=.008, p=.001), CRP did not mediate longitudinal psychosocial stress-memory associations because none of the Wave 1 psychosocial stressors were associated with Wave 2 CRP. Nonetheless, there were total effects of Wave 1 everyday discrimination (B= -.055, SE=.009, p<.001), neighborhood physical disorder (B= -.036, SE=.009, p<.001), and subjective societal status (B=.039, SE=.010, p<.001) on Wave 3 memory. Cross-sectional associations between more Wave 1 everyday discrimination and worse Wave 1 memory were stronger among Black participants (B= -.059, SE=.021, p=.004) compared to White participants (B= -.041, SE=.010, p<.001). Conclusions: Results do not provide evidence that CRP longitudinally mediates psychosocial stress-memory associations, but longitudinal associations between multilevel psychosocial stressors and memory support further study of pathways underlying these relationships. Results point to independent, unique effects of multilevel psychosocial stressors across interpersonal, community, and societal contexts on later memory in older adults. While cross-sectional findings are generally consistent with previous research and could be partially explained by compound disadvantage of multiple stressors that may increase Black participants’ risk for worse cognitive function, examining the mediating role of CRP may be more nuanced. Future research should examine alternative markers of inflammation that may be more sensitive to psychosocial exposures as well as additional pathways underlying effects of psychosocial stress on health disparities in cognitive aging.

Paper

02/15/2024
11:45 am - 01:15 pm
Room: West Side Ballroom - Salon 3

Paper Session 04: Cognitive Aging and Related Topics 1

Final Abstract #3

Is Systemic Inflammation a Mediator of Longitudinal Psychosocial Stress-Memory Associations in Black and White Older Adults?

Emily Morris, University of Michigan, Ann Arbor, United States
Ketlyne Sol, University of Michigan, Ann Arbor, United States
Kiana Scambray, University of Michigan, Ann Arbor, United States
Ji Hyun Lee, University of Michigan, Ann Arbor, United States
Jordan Palms, University of Michigan, Ann Arbor, United States
Laura Zahodne, University of Michigan, Ann Arbor, United States

Category: Aging

Keyword 1: chronic stress
Keyword 2: minority issues
Keyword 3: memory disorders

Objective:

Growing research has established that psychosocial stressors at the interpersonal, community, and societal levels are negatively associated with memory performance and partially explain Black-White memory disparities memory in older adulthood. However, little is known regarding specific pathways linking psychosocial stress with memory, particularly over time. Systemic inflammation, as measured by C-reactive protein (CRP), may be one relevant biophysiological pathway, given known associations between stress and inflammation, particularly among Black older adults. This study used a robust cross-lagged longitudinal mediation framework to identify whether systemic inflammation is a mechanism underlying multilevel psychosocial stress-memory associations, and whether associations differ across older Black and White adults.

Participants and Methods:

Participants included 15,382 adults (22% Black participants, 78% White participants) aged 51 and older from the 2010 and 2012 waves of the Health and Retirement Study (HRS). Participants completed measures of interpersonal (everyday discrimination), community (neighborhood physical disorder), and societal (subjective societal status) stress at baseline (Wave 1). Systemic inflammation was operationalized as the CRP concentration measured by a high-sensitivity assay of capillary blood collected at Wave 2, two years after Wave 1. A composite of immediate and delayed recall of a 10-item word list from Wave 3 was the outcome variable, measured four years after Wave 1. Cross-lagged mediation analyses examined whether Wave 2 CRP mediated associations between Wave 1 psychosocial stressors and Wave 3 memory, controlling for autoregressive pathways of CRP at Wave 1 and memory at Waves 1 and 2, covariates (age, sex, education, and wealth, measured at Wave 1), and study enrollment year. Race-stratified mediation models estimated associations in Black and White participants separately.

Results:

While higher Wave 2 CRP was associated with worse Wave 3 memory (B= -.024, SE=.008, p=.001), CRP did not mediate longitudinal psychosocial stress-memory associations because none of the Wave 1 psychosocial stressors were associated with Wave 2 CRP. Nonetheless, there were total effects of Wave 1 everyday discrimination (B= -.055, SE=.009, p<.001), neighborhood physical disorder (B= -.036, SE=.009, p<.001), and subjective societal status (B=.039, SE=.010, p<.001) on Wave 3 memory. Cross-sectional associations between more Wave 1 everyday discrimination and worse Wave 1 memory were stronger among Black participants (B= -.059, SE=.021, p=.004) compared to White participants (B= -.041, SE=.010, p<.001).

Conclusions:

Results do not provide evidence that CRP longitudinally mediates psychosocial stress-memory associations, but longitudinal associations between multilevel psychosocial stressors and memory support further study of pathways underlying these relationships. Results point to independent, unique effects of multilevel psychosocial stressors across interpersonal, community, and societal contexts on later memory in older adults. While cross-sectional findings are generally consistent with previous research and could be partially explained by compound disadvantage of multiple stressors that may increase Black participants’ risk for worse cognitive function, examining the mediating role of CRP may be more nuanced. Future research should examine alternative markers of inflammation that may be more sensitive to psychosocial exposures as well as additional pathways underlying effects of psychosocial stress on health disparities in cognitive aging.