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Introduction Prior research assessing self-reported or nocturnal sleep suggested that specific sleep traits (sleep restriction in the laboratory; poor sleep quality, sleep disorders) are associated with both pro and anti-inflammatory cytokine and C-Reactive Protein (CRP) levels. To extend prior research, we investigated associations between multiple dimensions of objectively assessed sleep health with both circulating and stimulated inflammatory markers in a diverse sample of older adults. Methods Participants in the Einstein Aging Study (EAS) were included (N=218, Mage=77.5 years, 6% female; 46% White, 38% Black, 14% Hispanic/other). A confirmatory factor analysis using wrist actigraphy sleep variables over 16 days yielded 6-component multi-dimensional sleep health facets: Regularity, Alertness/Sleepiness (daytime), Timing, Efficiency, Duration, and Rhythmicity. Inflammatory markers collected in the morning included CRP and both circulating markers reflecting current systemic inflammation, and lipopolysaccharide (LPS)-stimulated levels of (IL-1β, IL-4, IL-6, IL-8, IL-10, TNF𝛼), which reflect responses to an inflammatory challenge, an index of immune reactivity. Associations between each inflammatory marker and each sleep health facet were examined using linear regression, controlling for BMI, gender, age, education, ethnicity/race, number of health conditions, nocturnal hypoxemia, Oxygen Desaturation Index (ODI)≥15. Results Participants with more daytime sleepiness (i.e., higher number and longer duration of naps and lower activity level) had higher circulating IL-6 and CRP levels. Lower sleep efficiency was associated with lower levels of the anti-inflammatory circulating cytokine IL-4 and higher levels of stimulated IL-8 and TNF𝛼. Longer sleep duration was associated with higher levels of circulating IL-1β and CRP. Less rhythmicity across days was associated with higher levels of circulating IL-6. Nocturnal hypoxemia was associated with higher levels of CRP and stimulated IL-4, IL-8, and TNFα. We found no association between sleep timing and regularity and any inflammatory marker. Conclusion We observed that various sleep health facets are related to markers of inflammation and immune reactivity in older adults. This research also demonstrates the value of using 24-hour, device-based estimates of different sleep health facets relevant for immune function. Associations between 24-h sleep and inflammation are particularly important for older adults, who evidence more daytime sleepiness and less rhythmic sleep/active patterns in daily life. Support (if any) R01AG062622, P01AG003949, RF1AG056331-04

Novel opportunities to examine how life experiences connect to health and mortality through biological aging have increased due to the affordability of genomic analysis. Although epidemiological studies suggest associations between stress and accelerated biological aging, most if not all measures in the past have been global, data cross-sectional, and from primarily white samples. As part of a completed measurement study, a diverse sample (n=140, 25-65 years, Mage=47, 65% Female) provided detailed stress measures, including EMA and lifetime stress assessments, and consented to future analysis of their blood samples. We successfully used decade-old blood samples to estimate methylation-based epigenetic clocks and examined them within the context of various stress measures as a preliminary phase of a future longitudinal study. Additional whole genome sequencing will also allow for future work that incorporate continuous measures of genomic ancestry when examining lifetime discrimination-related stress, rather than simply testing for demographic group differences.

Prospective memory (PM) refers to our memory for future intentions, such as attending an appointment or taking medication. Research suggests that PM deficits can distinguish healthy older adults from those in early stages of dementia. However, limited work has examined PM and biological markers associated with pathological memory decline. The current study examined older adults’ everyday PM lapses and inflammation. Older dementia-free adults (n =237, Mage=76.86 years), enrolled in the ongoing Einstein Aging Study, completed a two-week ecological momentary assessment (EMA) as part of the first wave of data collection. Participants provided two blood samples (pre/post EMA) and self-reported daily PM lapses during nightly surveys. Inflammatory levels quantified from blood were averaged and included in regression analyses predicting total number of PM lapses (covarying for: age, education, race, health, BMI, depressive symptoms). Reporting more PM lapses was associated with higher circulating levels of interleukin [IL]-8 (p=.007); no significant associations emerged with C-reactive protein or other circulating or stimulated (ex-vivo) cytokines (IL-1β, IL-4, IL-6, IL-8, IL-10, TNF-a). Gender moderated the observed link between IL-8 and PM lapses (p=.015); specifically, higher levels of IL-8 were associated with more PM lapses among men (95%CI=[0.54, 4.72]) but not women (95%CI=[-1.56, 1.25]). Other researchers that found poor cognitive performance in association with elevated IL-8 have suggested that this relation may be indicative of neurodegeneration and future pathology. Future studies should continue to examine daily PM lapses and inflammation across genders to identify mechanisms through which these constructs may relate to neurodegeneration and dementia risk.