FROM JAMA NEUROLOGY
Elderly individuals who have excessive daytime sleepiness might be more susceptible to accumulation of an Alzheimer’s disease (AD) biomarker, results of a prospective, longitudinal cohort study suggest.
In the study, excessive daytime sleepiness (EDS) was associated with increased accumulation of beta-amyloid, an important biomarker of AD that manifests in early preclinical stages, wrote first author Diego Z. Carvalho, MD, and his colleagues at the Mayo Clinic, Rochester, Minn. The report was published online March 12 in JAMA Neurology .
This finding corroborates previous studies showing that EDS is a risk factor for dementia or cognitive decline, the authors said.
“It remains unclear whether EDS is a result of greater sleep instability, synaptic or network overload, or neurodegeneration of wakefulness-promoting centers,” Dr. Carvalho and colleagues wrote in their report. “However, participants with EDS were more vulnerable to AD pathologic processes.”
The prospective, longitudinal cohort analysis from Dr. Carvalho and his colleagues included 283 participants age 70 or older without a diagnosis of dementia who filled out a sleepiness assessment survey and underwent baseline and follow-up imaging studies as part of the Mayo Clinic Study of Aging.
All participants included in the analysis underwent at least two consecutive carbon 11–labeled Pittsburgh compound B PET (PiB-PET) scans. EDS, defined as a score of at least 10 on the Epworth Sleepiness Scale, was seen in 63 participants (22.3%), the researchers found.
At baseline, EDS was significantly associated with increased beta-amyloid accumulation in the anterior cingulate (P = .04), posterior cingulate-precuneus (P = .02), and parietal (P = .04) regions. The association between EDS and longitudinal beta-amyloid accumulation was most pronounced in participants who had global PiB positivity at baseline in anterior cingulate and cingulate-precuneus regions (P = .02 for both), they reported.
Findings of the study are consistent with a previous investigation of middle-aged participants without dementia, Dr. Carvalho and coauthors said in a discussion of the results. In that study, increased daytime somnolence was associated with increased beta-amyloid burden in regions including the precuneus and anterior cingulate. Daytime sleepiness in that study was measured using a different measure, the Sleep Scale, which was originally developed as part of the Medical Outcomes Study.
Further investigation of the link between EDS and beta-amyloid accumulation is needed. In particular, the researchers suggested that future studies might evaluate whether amyloid accumulation can be avoided through early recognition of EDS and subsequent treatment of the underlying sleep disorder.
The study was funded by grants from the National Institutes of Health and several foundations. Dr. Carvalho reported no disclosures related to the study. Many of his coauthors reported relationships with a variety of pharmaceutical companies developing therapies for Alzheimer’s.
SOURCE: Carvalho D et al., JAMA Neurol. 2018 Mar 12. doi: 10.1001/jamaneurol.2018.0049