Study: Excessive Daytime Sleepiness Linked to Alzheimer's Disease

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There is increasing evidence that there is some sort of association between sleep problems and dementias such as Alzheimer’s disease. This was further linked with a recent research study published in the journal Sleep by a group led by Adam Spira of Johns Hopkins University and Murat Bilgel, Luigi Ferrucci, Susan Resnick and Eleanor Simonsick of the National Institute on Aging (NIA)’s Intramural Research Program.

The researchers evaluated 124 community-dwelling patients in the Baltimore Longitudinal Study of Aging (BLSA) Neuroimaging Substudy. They were all cognitively healthy. They self-reported measurements of excessive daytime sleepiness (EDS) and napping, and then underwent PET scans of the brain to evaluate beta-amyloid plaque accumulation, one of the primary indications of Alzheimer’s disease.

The authors state in the study, “Disturbed sleep has emerged as a candidate risk factor for Alzheimer’s disease (AD). Multiple studies link indices of poor sleep to cognitive impairment and decline, and more recent studies link sleep disturbance to AD biomarkers.”

Their results found that people who reported shorter sleep duration and poorer sleep quality had greater beta-amyloid deposits. In fact, the older adults who reported feeling sleepy during the day when they wanted to be awake—a significant distinction between just feeling like taking a nap—were three times more likely to have beta-amyloid accumulation in their brains.

Of the BLSA, 50 percent were women and 21 percent were non-white. Approximately 24 percent had EDS and 29 percent took naps. The respondents with EDS were older than the majority without EDS. Nappers were generally older as well, more likely to be male, and had slightly higher education levels.

The authors state, “While not a direct correlation, the researchers see the results are further evidence that sleep problems and Alzheimer’s pathology may be connected. The exact mechanism that connects disturbed sleep with beta-amyloid buildup is unclear, but multiple studies have shown that people with dementia often experience sleep disturbances, and other studies have shown buildups of beta-amyloid in the brains of animals whose sleep was disturbed.”

The authors recognize several problems with their study, including the fact that the EDS and napping was self-reported. There also were no baseline beta-amyloid measurements. As a result, although provocative and consistent with other studies suggesting there’s a link between sleep disturbances and Alzheimer’s disease, the link and its mechanism are not clear-cut. The authors suggest four (at least) possibilities.

First, the EDS may derive directly from disturbed sleep and that it’s the disturbed sleep that causes accumulation of beta-amyloid.

Second, beta-amyloid deposits may cause EDS by limiting sleep duration or quality. “Although there is not yet evidence that interrupting this cycle by treating disturbed sleep resulting from beta-amyloid deposition slows Alzheimer’s disease progression,” the authors write, “this is an important area for investigation.”

Third, not just a marker of beta-amyloid accumulation, EDS might actually promote beta-amyloid clustering. However, the authors note there’s no pathway known for this, so it’s the least likely possibility.

And fourth, changes in circadian rhythms might play a role in all of the scenarios. “Circadian rest/activity rhythm alterations have been tied to an increased risk of mild cognitive impairment or dementia diagnosis and preclinical amyloid deposition in humans,” the authors wrote.

The study suggests that screening for EDS might help identify people who are at elevated risk of Alzheimer’s. They also point out that although a healthy diet and mental and physical exercise are noted strategies for reducing the risk of dementia, quantity and quality of sleep hasn’t been emphasized enough.

They wrote, “The study showed that a simple yes or no question on if people felt drowsy or fell asleep in the daytime when they wanted to be awake was effective to screen those at risk for having beta-amyloid deposits in their brains. While not everyone who has Alzheimer’s disease pathology goes on to develop cognitive problems, adding this question to routine clinical screenings could help identify people who should consider follow-up testing for Alzheimer’s and related dementias risk.”

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