Lack of sleep accelerates brain damage and causes dementia

Researchers have long known that poor sleep is associated with Alzheimer’s, but little is known about how sleep disruption causes the disease. Recently, researchers at the University of Washington School of Medicine found that sleep deprivation increases the level of Tau, a key protein in Alzheimer’s disease, through studies in mice and humans. Moreover, in a subsequent study of mice, the team found that lack of sleep accelerated the spread of harmful Tau protein masses in the brain – a precursor to brain damage and a critical step in dementia.

The findings, published in the January 24 issue of Science, suggest that sleep deprivation may trigger Alzheimer’s disease and point out that good sleep habits help keep the brain healthy.

“The interesting thing about this research is that it suggests that real-life factors such as sleep may affect the rate at which the disease spreads in the brain,” said David Holtzman, head of the Department of Neurology at the University of Washington School of Medicine. “We already know that sleep problems and Alzheimer’s disease are partly linked to another Alzheimer’s disease protein, beta-amyloid (Aβ), but this study suggests that sleep disruption The destructive Tau protein rapidly increases and promotes its spread.”

Tau proteins are usually found in the brain – including the brains of healthy people – but under certain conditions, the proteins will clump together and entangle into clumps that damage surrounding tissues, potentially causing cognitive decline. Recent studies have shown that levels of Tau protein are high in the brains of older people with poor sleep. However, it is unclear whether sleep deprivation directly forces Tau levels to rise, or whether the two are otherwise associated. To find out, Holzman and colleagues measured Tau protein levels in mice and humans during normal sleep and sleep disruption.

The mouse is a nocturnal animal. The researchers found that when mice were more awake and active, the level of Tau protein in their brain cells was about twice as high as during the day, and mice slumber more often during the day. Disturbing sleep in mice during the day can result in a doubling of daytime Tau protein levels.

Almost the same results have been observed in humans. The researchers extracted cerebrospinal fluid (filled in the ventricular system, subarachnoid space, and colorless transparent fluid in the central canal of the spinal cord) after eight nights of normal sleep, and extracted them again after they had not slept all night… The researchers found that overnight sleep deprivation caused an increase in Tau protein levels of about 50%.

Staying up late can make you feel stressed and irritable, and more likely to fall asleep when you have a chance. Although it is difficult to judge the mood of mice, they will rebound and sleep more after a day without sleeping. To rule out the possibility of changes in Tau protein levels caused by stress or behavioral changes, the researchers developed genetically engineered mice that were kept awake for hours by injecting harmless compounds. When the compound is depleted, these mice return to a normal sleep-wake cycle without showing any stress or signs of additional need for additional sleep.

Using these mice, the researchers found that maintaining a long-term awake resulted in elevated levels of Tau protein. All of these findings suggest that the brain releases the Tau protein through normal thought and action during waking, and then gradually releases during sleep, allowing the Tau protein to be cleared. Sleep deprivation disrupts this cycle, causing the Tau protein to accumulate and more likely to form harmful masses.

For people with Alzheimer’s disease, Tau protein masses tend to appear in areas of the brain that are important for memory—the hippocampus and the entorhinal cortex—and then spread to other brain regions. As the Tau protein tangles and affects more areas, it becomes increasingly difficult for the brain to think clearly.

To investigate whether the diffusion of the Tau protein mass was affected by sleep, the researchers “sowed” the smaller Tau protein mass into the hippocampus of the mice and then kept the mice awake for long periods of time each day. Another group of mice allowed to sleep at any time after injection of the Tau protein mass. After 4 weeks, in the brains of sleep-deprived mice, the degree of diffusion of Tau protein mass was much more severe than that of the mice in the adequate rest group. It is worth noting that the areas of new clumps in the brains of these mice are the same as those affected by Alzheimer’s disease.

“Sleeping well is something we should all try to do,” Holtzman said. “Our brain needs time to recover from the stress of the day. We don’t know how to get enough sleep during the process of growing up. Whether it can prevent Alzheimer’s disease, but this is no harm, and the data from this and other studies suggest that adequate Alzheimer’s can even help to delay and slow the progression of the disease if Alzheimer’s disease has begun.”

The researchers also found that sleep disruption increases the release of synuclein, a marker of Parkinson’s disease. Like Alzheimer’s patients, people with Parkinson’s disease usually have sleep problems.


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