A new study from UC San Francisco found some people are gifted with genes that pack the benefits of slumber into an efficient time window, keeping them peppy on only four or six hours of sleep a night.
In addition, these “elite sleepers” show psychological resilience and resistance to neurodegenerative conditions that may point the way to fending off neurological disease.
The study is published in iScience and was conducted by Louis Ptacek et al.
For over a decade, the team has been studying people with Familial Natural Short Sleep (FNSS), the ability to function fully on—and have a preference for—four to six hours of sleep a night.
They’ve shown that it runs in families and, thus far have identified five genes across the genome that play a role in enabling this efficient sleep.
In the study, the team tested the hypothesis that elite sleep can be a shield against neurodegenerative disease.
They bred mice that had both short-sleep genes and genes that predisposed them to Alzheimer’s and found that their brains developed much less of the hallmark aggregates associated with dementia.
To confirm their findings, they repeated the experiment using mice with a different short-sleep gene and another dementia gene and saw similar results.
Researchers believe that similar investigations of other brain conditions would show the efficient-sleep genes conferring comparable protections. improving people’s sleep could delay the progression of disease across a whole spectrum of conditions.
Understanding the biological underpinnings of sleep regulation could identify drugs that will help ward off problems with sleep disorders.
In addition, improving sleep in healthy people may sustain wellbeing and improve the quality of time.
Related: This healthy diet may strongly prevent memory loss and dementia
Previous studies have found a strong link between sleep and Alzheimer’s disease.
For example, a study from The Pennsylvania State University found evidence of sleep-dependent low-frequency (<0.1 Hz) global brain activity in the clearance of Alzheimer’s disease-related toxin buildup.
This neuronal activity was more strongly linked with cerebrospinal fluid flow in healthy controls than higher-risk groups and patients, and the findings could serve as a potential imaging marker for clinicians in evaluating patients.
The development of Alzheimer’s disease is believed to be driven by the buildup of the toxic proteins amyloid-β and tau in the brain.
The brain’s glymphatic system plays a crucial role in clearing these toxins.
In that study, the team examined 118 people in the Alzheimer’s Disease Neuroimaging Initiative project. They measured this brain activity and cerebrospinal fluid flow as well as looking at behavioral data.
The researchers found the strength of the connection between brain activity and cerebrospinal fluid flow was weaker in people at a higher risk or who had already developed Alzheimer’s disease.
Additionally, this weaker connection was linked to higher levels of amyloid-β and disease-related behavioral measures two years later.
This suggests an important role for sleep-dependent global brain activity in the clearance of brain waste, and its connection to cerebrospinal fluid flow could be helpful as a future marker for clinical evaluation.
The study findings linked the coupling between the resting-state global brain activity and cerebrospinal fluid flow to Alzheimer’s disease pathology.
The finding highlights the potential role of low-frequency (<0.1 Hz) resting-state neural and physiological dynamics in neurodegenerative diseases, presumably due to their sleep-dependent driving of cerebrospinal fluid flow to wash out brain toxins.
Another study from Washington University in St. Louis found that for common people, both short and long sleepers experienced greater cognitive decline than people who slept a moderate amount, even when the effects of early Alzheimer’s disease were taken into account.
The finding suggests that there is a middle range, or ‘sweet spot,’ for total sleep time where cognitive performance was stable over time. Short and long sleep times were associated with worse cognitive performance.
In the study, the team tracked cognitive function in a large group of older adults over several years and analyzed it against levels of Alzheimer’s-related proteins and measures of brain activity during sleep.
In total, they obtained sleep and Alzheimer’s data on 100 participants whose cognitive function had been monitored for an average of 4 1/2 years.
Most (88) had no cognitive impairments, 11 were very mildly impaired, and one had mild cognitive impairment. The average age was 75 at the time of the sleep study.
The researchers found a U-shaped link between sleep and cognitive decline.
Overall, cognitive scores declined for the groups that slept less than 4.5 or more than 6.5 hours per night—as measured by EEG—while scores stayed stable for those in the middle of the range.
EEG tends to yield estimates of sleep time that are about an hour shorter than self-reported sleep time, so the findings correspond to 5.5 to 7.5 hours of self-reported sleep.
The U-shaped link held true for measures of specific sleep phases, including rapid-eye-movement (REM), or dreaming, sleep; and non-REM sleep.
The findings suggest that sleep quality may be key, as opposed to simply total sleep.
If you care about dementia, please read studies about antibiotic drug that could effectively treat common dementia, and how unhealthy blood pressure increases your dementia risk.
For more information about brain health, please see recent studies about common gut disease linked to doubling in dementia risk, and results reveal a new, complex form of dementia.
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