Excessive Daytime Sleepiness Linked to Elevated β-Amyloid Accumulation in Elderly Persons
Aging and excessive daytime sleepiness are correlated with reduced cognition in elderly individuals.
Elevated daytime sleepiness (EDS) in elderly persons without dementia may be linked to longitudinal β-amyloid accumulation, according to a study published in JAMA Neurology.
Diego Z. Carvalho, MD, of the Department of Neurology at the Mayo Clinic in Rochester, Minnesota, and associates conducted a prospective analysis to determine whether there is an association between EDS and increased regional β-amyloid accumulation.
A total of 2900 volunteers were included and asked to complete a survey regarding sleepiness at the start of the analysis; 74.9% of volunteers agreed to carbon 11-labeled Pittsburgh compound B positron emission tomography (PiB-PET).
Volunteers selected (n= 283) were 70 years or older (average age, 77.1), did not have dementia after completion of sleepiness surveys, and completed at least 2 PiB-PET scans; 13.7% of patients had a comorbid neurologic disorder and were excluded from further assessment.
The primary outcome was the Epworth Sleepiness Scale score, used to measure EDS; scores of at least 10 indicated EDS. In addition, the investigators measured the variation in regional β-amyloid accumulation between the 2 PiB-PET scans in vulnerable loci.
Of the 283 volunteers, 63 (22.3%) had EDS. At baseline, a significant correlation was detected between EDS and elevated regional β-amyloid accumulation at the anterior cingulate (B coefficient, 0.031), posterior cingulate-precuneus (B coefficient, 0.038), and parietal (B coefficient, 0.033) loci.
The researchers reported the strongest correlations in patients who had global PiB positivity at the anterior cingulate (B coefficient, 0.065) and cingulate-precuneus (B coefficient, 0.068) at baseline.
“Baseline EDS was associated with increased longitudinal Aβ accumulation in elderly persons without dementia, suggesting that those with EDS may be more vulnerable to pathologic changes associated with Alzheimer disease,” the authors wrote. “Further work is needed to elucidate whether EDS is a clinical marker of greater sleep instability, synaptic or network overload, or neurodegeneration of wakefulness-promoting centers.”
Carvalho DZ, St Louis EK, Knopman DS, et al. Association of excessive daytime sleepiness with longitudinal β-amyloid accumulation in elderly persons without dementia. JAMA Neurol. 2018;75(6):672–680.