The Link Between Daytime Sleepiness and Risk of Dementia

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Given the link between sleep and health, it would seem a worthwhile consideration to see if there’s an association between daytime sleepiness and the risk of developing dementia. A 2018 study published in the Journal of the American Medical Association (JAMA) examined this possible link.

The study identified individuals who appeared free of dementia at the time they were recruited. The subjects were already enrolled in the Mayo Clinic Study of Aging, a longitudinal study based in Olmsted County, Minnesota. Of the 2,900 total subjects, 2,172 agreed to undergo positron emission tomography (PET) scans. Among that group were 283 participants 70 years or older, who had no diagnosis of dementia at baseline of the study. There are some key questions that are worth exploring with regards to this particular study.

How did the researchers determine the ‘presence of dementia’ in the participants?

The objective evidence of dementia currently being used is to identify the presence of amyloid protein surrounding the fibers of the brain. In this study, they looked at more than 2,000 patients based in Minnesota, and assessed them with PET scan technology that used a carbon-labeled compound that selects beta amyloid. Then using standard uptake value (SUV), they quantified the activity of the labeled compound to identify levels of the amyloid present in each brain.

How did they determine if the subjects had excessive daytime sleepiness?

To measure the level of daytime sleepiness, they used the Epworth Sleepiness Scale (ESS). This is a subjective test where the individual ranks the tendency to doze off during eight different life situations.

They found a strong association between ESS scores that suggested the presence of excessive daytime sleepiness and accumulation of beta amyloid in three areas of the brain involved in cognitive reasoning and function.

This finding was identified after adjusting for age, education, and the presence of the gene associated with Alzheimer’s disease called apolipoprotein E. Even in those subjects who did not have presence of frank dementia, the link suggested that they were more vulnerable to developing Alzheimer’s disease.

As a sleep medicine expert, I think it’s worth asking if there’s an association between dementia and the consequences of sleep instability. Lack of sleep may cause overload of the synapses of the neurons in the brain, leading to neurodegeneration of wakeful-promoting centers in the brain. An even more important question is: Would diagnosing and treating sleep disorders early prevent the consequences that, based on this study, appear linked to dementia?

The association between age-dependent dementia and sleep disturbances is well-known and has a basis through a few identified pathways.

In one pathway there are changes in sleep quality and duration in elderly individuals diagnosed with dementia, and these individuals seem to exhibit more disruptive sleep compared to age-matched controls. This finding is not exclusive to the dementia associated with accumulation of beta amyloid. There’s also been an association shown with neurological disorders that involve another “protein of neural degeneration” called synuclein. The best examples of these conditions are Parkinson’s disease and another disorder of dementia called Lewy body dementia.

In another pathway, there are changes in the sleep architecture in older individuals. As we age, sleep becomes less deep and more fragmented. There are more arousals and increased number of sleep stage shifts due to the frequent arousals. The percentage of time in rapid eye movement (REM) stage decreases. Decrease in REM has been associated with poorer cognition. These changes become more pronounced in those with dementia because of the underlying neurodegenerative process of the disease itself.

In yet another pathway, there are changes in circadian rhythm. The most common process is advanced sleep schedule disorder, where elderly individuals go to sleep early in the night and awaken in the middle of the night and are then unable to fall back asleep. In seniors with dementia, these changes become more pronounced. With the complication of more irregular behavior patterns (due to dementia), this brings about changes in body core temperature that can disrupt circadian rhythm. Sundowning — a late-in-the-day state of confusion associated with restless and uncontrollable behavior — can also disrupt circadian rhythm.

Patients with dementia have also shown dysregulation in the secretion of melatonin, which is supposed to be secreted according to a schedule set by the circadian cycle.

Given all of these associations between excessive daytime sleepiness and the development of dementia one can wonder: What came first and which process causes the other?

It would be more accurate to say that both processes (dementia and effects of impaired sleep) feed on each other.

There’s a reason why the brain functions optimally in a normal circadian cycle. It allows parts of the brain to reset and repair while other parts are at work. Having excessive neuronal activity without rest carries negative consequences. There are also other risk factors and lifestyle habits associated with accumulation of beta amyloid.

The findings of this study suggest that the consequences of sleep instability, daytime sleepiness, and dementia manifested by amyloid deposition, occur concurrently.

The approach to preventing this association is not as simple as “just” treating insomnia. Elderly individuals may not be aware of the process of sleep impairment progressing. As they adjust to life with irregular schedules and less interaction with others, lack of exposure to sunlight at the right time of day, and feeling the effects of (many) medications, the deterioration in brain function may be their “new normal.” Some other helpful tips:

  • Certainly caregivers should try to help achieve a regular routine with activities and exposure to light during the day.

  • A period of relaxation at night to prepare for sleep can also help.

  • Stimulation of the brain with activities that require thinking is paramount to limiting dementia.

  • Making an effort to integrate the treatment and medications dispensed by different doctors who are unaware of each other and making sure medications are necessary and at the right dosages is crucial. The primary care physician should coordinate with the caregiver.

Paying attention to early warning signs of disturbed sleep and dementia are crucial to intercepting these processes or at minimum, slowing them down.

See more helpful articles:

New Guidelines for Pharmacologic Treatment of Chronic Insomnia

A Guide to Sleep Testing

Improving Sleep to Battle Cognitive Decline: A New Approach