In:
Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 1 ( 2024-01-9)
Kurzfassung:
Both short and long sleep duration were previously associated with incident dementia, but underlying mechanisms remain unclear. We evaluated how self-reported sleep duration and its change over time associate with (A)myloid, (T)au, (N)eurodegeneration, and (V)ascular neuroimaging markers of Alzheimer disease. Methods Two Framingham Heart Study overlapping samples were studied: participants who underwent 11 C-Pittsburg Compound B amyloid and 18 F-flortaucipir tau PET imaging and participants who underwent an MRI. MRI metrics estimated neurodegeneration (total brain volume) and cerebrovascular injuries (white matter hyperintensities [WMHs] volume, covert brain infarcts, free-water [FW] fraction). Self-reported sleep duration was assessed and split into categories both at the time of neuroimaging testing and approximately 13 years before: short ≤6 hours. average 7–8 hours, and long ≥9 hours. Logistic and linear regression models were used to examine sleep duration and neuroimaging metrics. Results The tested cohort was composed of 271 participants (age 53.6 ± 8.0 years; 51% male) in the PET imaging sample and 2,165 participants (age 61.3 ± 11.1 years; 45% male) in the MRI sample. No fully adjusted association was observed between cross-sectional sleep duration and neuroimaging metrics. In fully adjusted models compared with consistently sleeping 7–8 hours, groups transitioning to a longer sleep duration category over time had higher FW fraction (short to average β [SE] 0.0062 [0.0024] , p = 0.009; short to long β [SE] 0.0164 [0.0076] , p = 0.031; average to long β [SE] 0.0083 [0.0022] , p = 0.002), and those specifically going from average to long sleep duration also had higher WMH burden (β [SE] 0.29 [0.11] , p = 0.007). The opposite associations (lower WMH and FW) were observed in participants consistently sleeping ≥9 hours as compared with people consistently sleeping 7–8 hours in fully adjusted models (β [SE] −0.43 [0.20] , p = 0.028; β [SE] −0.019 [0.004] , p = 0.020). Each hour of increasing sleep (continuous, β [SE] 0.12 [0.04] , p = 0.003; β [SE] 0.002 [0.001] , p = 0.021) and extensive increase in sleep duration (≥2 hours vs 0 ± 1 hour change; β [SE] 0.24 [0.10] , p = 0.019; β [SE] 0.0081 [0.0025] , p = 0.001) over time was associated with higher WMH burden and FW fraction in fully adjusted models. Sleep duration change was not associated with PET amyloid or tau outcomes. Discussion Longer self-reported sleep duration over time was associated with neuroimaging biomarkers of cerebrovascular pathology as evidenced by higher WMH burden and FW fraction. A longer sleep duration extending over time may be an early change in the neurodegenerative trajectory.
Materialart:
Online-Ressource
ISSN:
0028-3878
,
1526-632X
DOI:
10.1212/WNL.0000000000207807
Sprache:
Englisch
Verlag:
Ovid Technologies (Wolters Kluwer Health)
Publikationsdatum:
2024
