Nighttime behaviors, but not insomnia, correlates with cognition and biomarkers of dementia

Abstract

AbstractBackgroundWhile sleep disturbances appear to be risk factors in the progression of Alzheimer’s disease (AD) and other dementias, little is known about the prevalence across dementia severity and the potential influence on the trajectory of cognitive decline.MethodWe used the prospective National Alzheimer Coordinating Center Uniform Data Set to evaluate the hypotheses that the prevalence of insomnia differs by definition and by stage of cognitive impairment, that certain sleep features track with established biomarkers of AD, and that longitudinal changes in sleep disorders affect cognition and AD biomarkers. We conducted cross‐sectional analyses to determine the prevalence of clinician‐determined insomnia and nighttime behaviors (nighttime restlessness, agitation, daytime sleepiness) in normal, mild cognitive impairment (MCI), and demented individuals, as defined by Montreal Cognitive Assessment (MoCA) cut‐off scores obtained during the patient’s first visit. We evaluated mean MoCA scores, hippocampal volumes, and CSF phosphorylated tau:beta amyloid ratios obtained near the first visit using Analysis of Variance (ANOVA) with age as a covariate. In longitudinal evaluations, we classified changes in insomnia and nighttime behaviors as “none”, “remitted”, “acquired”, or “steady” between the first and last visits. Similar changes in MoCA scores and hippocampal volumes were assessed with repeated‐measure ANOVA.ResultThe prevalence of clinician‐identified insomnia at initial visits was 15%, 17%, and 13% for normal, MCI, and dementia groups respectively. Prevalence of clinician‐identified nighttime behaviors was 13%, 19%, and 27% respectively. Insomnia was significantly associated with higher MoCA scores, larger hippocampal volumes, and higher pTau:Beta values, indicating those with clinician‐identified insomnia had better cognition and less neurodegeneration than individuals who clinicians identified to be without insomnia. In contrast, the presence of nighttime behaviors were associated with significantly worse cognition, smaller hippocampal volumes, and lower pTau:Beta. Similar findings were seen between longitudinal associations of sleep disorders and cognition and hippocampal volumes.ConclusionOur findings suggest that the clinician determination of insomnia may be under‐recognized in patients with cognitive impairment seen in memory disorders clinics, and that nighttime behaviors especially when reported by family members may better reflect sleep disturbances, the biological underpinnings of AD, and have diagnostic specificity in AD over insomnia.