Excessive daytime sleepiness was linked to an increase in longitudinal beta amyloid accumulation among elderly adults without dementia, indicating excessive daytime sleepiness may be a risk factor for dementia, according to study findings.
“Excessive daytime sleepiness in this population has detrimental consequences. Several longitudinal studies have shown an association between [excessive daytime sleepiness] and an increased risk of dementia,” Diego Z. Carvalho, MD, department of neurology, Mayo Clinic, and colleagues wrote in JAMA Neurology. “However, the neurobiological mechanisms underlying this association remain unclear.”
Researchers conducted a prospective analysis to determine the effect of excessive daytime sleepiness at baseline on longitudinal increase in regional beta amyloid accumulation in 283 participants aged 70 years or older without dementia enrolled in a longitudinal population-based study.
Participants completed surveys asking about sleepiness at baseline and underwent at least two consecutive carbon 11–labeled Pittsburgh compound B positron emission tomography (PiB-PET) scans from Jan. 1, 2009, through July 31, 2016. The investigators measured excessive daytime sleepiness (defined as an Epworth Sleepiness Scale score of 10 or higher) and the change in beta amyloid levels between the two scans in the prefrontal, anterior cingulate, posterior cingulate-precuneus and parietal regions. Adjustment was made for confounders.
Excessive daytime sleepiness was associated with an increase in longitudinal beta amyloid accumulation among elderly adults without dementia, study findings revealed.
Overall, 63 participants (22.3%) had excessive daytime sleepiness. Carvalho and colleagues found that participants with excessive daytime sleepiness at baseline showed increased regional beta amyloid accumulation in the following beta amyloid-susceptible regions: the anterior cingulate (B coefficient = 0.031; 95% CI, 0.001-0.061; P = .04), posterior cingulate-precuneus (B coefficient = 0.038; 95% CI, 0.006-0.069; P = .02), and parietal (B coefficient = 0.033; 95% CI, 0.001 0.065; P = .04) regions. Furthermore, the relationship between sleepiness and longitudinal beta amyloid growth was stronger in elderly adults with global PiB positivity in the anterior cingulate (B coefficient = 0.065; 95% CI, 0.010-0.118; P = .02) and cingulate-precuneus (B coefficient = 0.068; 95% CI, 0.009-0.126; P = .02) regions at baseline.
“This finding supports previous literature suggesting that [excessive daytime sleepiness] is a risk factor for cognitive decline or dementia,” Carvalho and colleagues wrote. “Further investigations should assess determinants of [excessive daytime sleepiness] in elderly persons without dementia and whether early recognition of [excessive daytime sleepiness] and treatment of potential underlying sleep disorders can reduce amyloid accumulation in this vulnerable group.”
In a related editorial, Joseph R. Winer, MA, department of psychology, University of California, Berkeley, and Bryce A. Mander, PhD, department of psychiatry and human behavior, University of California, Irvine, wrote that this study provides important evidence that supports sleep disturbance as a risk factor for Alzheimer’s disease.
“This study and others present evidence that poor sleep quality may be an early warning sign of [Alzheimer’s disease]-related processes,” Winer and Mander wrote. “Although a better understanding of the role of sleep in the [Alzheimer’s disease] cascade could soon lead to effective sleep-based therapies, at present, maintaining healthy sleep and treating clinical sleep disorders must be a current priority for mental health in older adults.” – by Savannah Demko
Disclosures: Carvalho reports no relevant financial disclosures. Please see the full study for all other authors’ relevant financial disclosures. Winer and Mander report no relevant financial disclosures.