Self‐report sleep duration associates with plasma Aβ42/40 rate of change in late middle‐aged, African American Adults

Background Sleep abnormalities may play a prominent role in the pathogenesis or exacerbation of Alzheimer’s disease (AD). is considered modifiable target for prevention and treatment. Racial sleep health disparities exist, contribute to disproportionately increased risk developing AD associated with being African American. Yet, relationships between pathophysiology American individuals are under-studied. This investigation was designed address research gaps by evaluating associations self-report duration, disturbances, daytime sleepiness change plasma-derived amyloid β 42/40 ratio (Aβ42/40) an sample. Method Archival data from participants enrolled Wisconsin Registry Prevention study Disease Research Center were utilized. Data included Medical Outcomes Study Scale (MOS-Sleep), Epworth Sleepiness (ESS), demographic information. duration determined MOS-Sleep #2, disturbances captured related subscale (SLPD4), ESS assessed sleepiness. Participants provided plasma samples across multiple timepoints. PrecivityADTM assays quantified Aβ42/40. Aβ42/40 rate (Aβ42/40_ROC) computed follow-up collections serve as primary outcome measure. Aβ42/40_ROC difference first collection divided years collections. Linear mixed-effects models Aβ42/40_ROC. Observations nested within participant. Fully adjusted age at collection, gender, BMI, education, parental history dementia, APOEe4 carrier status. Result 339 143 participants. Women 70.8% collections, average = 66.6 ± 8.84 years, -0.0005 0.003, 6.35 1.00 hours. significantly fully model (β -0.0005; SE 0.0002; p 0.02) (Figure 1). Associations SLPD4 nonsignificant. Conclusion Longer steeper reduction Aβ42/40, biomarker pathology. Further necessary clarify components changes AD-related biomarkers adults identify focal factors interventional strategies.