Lack of sleep accelerates brain damage in Alzheimer's: study


By studying mice and people, researchers at the University of Washington School of Medicine in St. Louis found that lack of sleep increases tau levels of Alzheimer's disease, and insomnia accelerates the spread of toxic substances through the brain. Groups of tau, a harbinger of brain damage and a decisive step on the road to dementia.

To find out if lack of sleep was directly pushing tau levels up, the researchers measured tau levels in normal and disrupted sleep, and found that tau levels in the fluid around the brain cells were approximately twice as high at night, when the animals were more awake and active, than during the day, when the rats dozed more often.Disturbing the rest of the mice during the day caused daytime tau levels to double.

The same effect was observed in people. The cerebrospinal fluid that researchers of eight people obtained after a normal night of sleep and again after waking up all night shows that one night of insomnia caused tau levels to increase by 50%.

To rule out the possibility of stress or behavioral changes that explain changes in tau levels, the researchers created genetically modified mice that could be kept awake for hours by injecting them with an innocuous compound. When the compound disappears, the mice return to their normal sleep-wake cycle, with no signs of stress or apparent desire to sleep more.

Using these mice, the researchers found that staying awake for prolonged periods causes tau levels to increase. Taken together, the results suggest that tau is routinely released during waking hours by the normal business of thinking and doing, and then this release decreases during sleep, allowing tau to be eliminated. Sleep deprivation interrupts this cycle, which allows tau to accumulate and increases the likelihood that the protein will start to accumulate in harmful entanglements.

In people with Alzheimer's disease, tau tangles tend to emerge in parts of the brain that are important to memory, the hippocampus, and the entorhinal cortex, and then spread to other regions of the brain.

To study whether the spread of tau nodes is affected by sleep, researchers have planted the hippocampus of mice with small tau groups and then kept the animals awake for long periods of time every day. A separate group of mice was also injected with tau entanglements but were allowed to sleep when they wanted. After four weeks, tau nodes spread more in sleep-deprived mice than in their resting counterparts. In particular, new nodes appeared in the same affected brain areas in people with Alzheimer's.

The researchers also found that sleep disruption increased the release of the protein synuclein, a hallmark of Parkinson's disease. People with Parkinson's often have trouble sleeping, such as people with Alzheimer's.

"Sleeping well tonight is something we should all try to do," said study lead author David Holtzman, a professor and head of the university's Department of Neurology. "Our brains need time to recover from the stress of the day. We still do not know if getting enough sleep as people age will protect against Alzheimer's disease, but that can not hurt, and this and other data suggest they can help to slow down and slow down the disease process if it has already begun.


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