Mechanisms of sleep deficiency and effects on brain injury and neurocognitive functions among older blacks - Project Summary
Translational studies showing a mechanistic interplay between Alzheimer’s disease (AD) pathogenesis and
sleep/circadian disruption has renewed interest in the maxim ‘sleep is of the brain, by the brain, and for the
brain’. Relative to adults sleeping well, those exhibiting sleep deficiency (SD), defined as poor sleep, sleep
apnea, and/or circadian misalignment, have greater AD risk (OR=1.55), cognitive decline (OR=1.68), or
preclinical AD (OR=3.78). Since SD is observed early in the course of AD, it constitutes a prime target for
prevention. Notwithstanding successes in delineating the mechanisms and functions of sleep, a critical gap
remains in elucidating factors undergirding sleep disparities among blacks, marked by a greater AD risk
burden. Blacks also shoulder a greater sleep burden as evidenced by a higher prevalence of the main SD
indices, which are linked to increased vascular risks, inflammation, brain injury, and cognitive impairment.
The multi-disciplinary team will utilize innovative dynamic and geospatial modeling in a multi-level
framework to delineate the psychosocial and environmental determinants of SD and its putative effects on
the brain health of older blacks. We will leverage the success of the NYU Sleep Disparity Workgroup,
comprising investigators with expertise in aging research, translational sleep and circadian sciences, brain
health, health disparities, and geospatial and multi-level dynamic modeling. We will leverage the social
capital and assets of our Community Steering Committee to enroll 504 blacks (60-75 years) from traditional
and non-traditional venues to capture study endpoints. We will investigative the following aims: 1) To
ascertain the psychosocial (social/emotional support, mood, discrimination, attitudes) and environmental
(household [density, noise, air quality, light, and temperature], socioeconomic position, social capital,
neighborhood [built environment]) factors that are associated with SD; 2) To assess effects of SD on
markers of brain injury (Hcy, NFL, GFAP, Tau & Amyloid-β peptides) and on neurocognitive functions
(attention, language, memory, and executive function using the Preclinical Alzheimer Cognitive Composite
and Trail Making Test). The contributions of vascular risk (obesity, BP, lipid, and glucose/HbA1C) and
inflammation (IL-6, IL-10, and TNF-α) will be weighted; 3) To characterize blacks who are at increased risk
of SD using Bayesian machine-learning modeling and forecast through Agent-Based modeling which
amalgamation of psychosocial and environmental changes will lead to a reduced SD burden and related
brain health profile among older blacks over time (5, 10, & 20 yrs.). The investigative team will use novel
home-based digital recorders, innovative brain health biomarkers, geospatial analytics and dynamic
systems modeling to describe the mechanisms of SD and delineate their potential role in explaining
observed disparities in markers of brain health of older blacks.
