Tau and amyloid PET associations with impaired sleep and 24‐hour rhythms across aging and neurodegenerative disease.

Autor: Winer, Joseph R., Romero, America, Lok, Renske, Vossler, Hillary, Young, Christina B., Anders, David, Shen, Bin, Morales, Aimara Pacheco, Davidzon, Guido, Henderson, Victor, Poston, Kathleen L., Zeitzer, Jamie M, Mormino, Elizabeth C.
Zdroj: Alzheimer's & Dementia: The Journal of the Alzheimer's Association; Dec2023 Supplement 17, Vol. 19, p1-3, 3p
Abstrakt: Background: Disrupted sleep and fragmentation of sleep‐wake rhythms are common in the context of healthy aging as well as in neurodegenerative disease. As wearable devices become increasingly popular among older adults, there is a growing need to understand how metrics of sleep‐wake behavior might be able to identify neurodegenerative disease and differentiate disease etiology and severity. Method: Participants (n = 145) from the Stanford Alzheimer's Disease Center (ADRC) and the Stanford Aging and Memory Study (SAMS) were recruited for 14 days of at‐home actigraphy (wrist‐worn accelerometry) data collection. A subset of participants received 18F‐PI‐2620 and 18F‐florbetaben PET scans to assess tau and amyloid burden. The cohort included cognitively normal older adults (healthy controls, HC), patients with Alzheimer's disease (AD) spectrum, and patients on the Lewy body (LB) disease spectrum. Actigraphy analyses focused on nocturnal sleep efficiency, 24‐hour diurnal amplitude, and 24‐hour activity fragmentation (intradaily variability, IV). Amyloid burden was quantified in centiloids and tau burden was quantified as 18F‐PI‐2620 SUVR within bilateral inferior temporal cortex. The Neuropsychiatric Inventory Questionnaire (NPI‐Q) was used as a measure of neuropsychiatric symptom severity. Result: LB patients had lower 24‐hour activity levels relative to AD and HC participants, as measured by diurnal amplitude (W's≥650, p's<0.01; Fig 1A & B). AD patients had marginally higher IV relative to HC (W = 1084.5, p<0.1; Fig 2A & B), whereas sleep efficiency was comparable across etiologies and cognitive status (Fig 1C). Higher IV was associated with higher NPI‐Q scores in cognitively impaired patients (rho = 0.31, p = 0.03; Fig 2C). Greater amyloid burden was associated with lower diurnal amplitude in HC and AD (rho = ‐0.29, p = 0.02; Fig 3A). Inferior temporal tau was associated with sleep efficiency both within HC and AD (rho = ‐0.28, p = 0.07; Fig 3B) and in all amyloid‐positive participants (rho = ‐0.41, p = 0.02; Fig 3C). Conclusion: These findings suggest that sleep and 24‐hour rhythms show meaningful variation across individuals and are associated with AD and LB disease severity. While sleep efficiency and IV did not robustly differ between AD and LB groups, the measures were associated with disease‐related features such as biomarkers of amyloid and tau pathology and neuropsychiatric symptoms. [ABSTRACT FROM AUTHOR]
Databáze: Supplemental Index