Insomnia threatens Alzheimer's
A single sleepless night increased the amount of beta-amyloid in the blood
A group of scientists led by Matthew Walker from the University of California at Berkeley examined 26 elderly people and found that chronic sleep deficiency is associated with a deterioration in the transformation of short-term memories into long-term memory and is accompanied by the accumulation of beta-amyloids in the brain, proteins found in the brains of patients with Alzheimer's type dementia. The corresponding work is published in Nature Neuroscience (Benedict et al., Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men), and its summary can be found on the university's website.
Using a combination of positron emission tomography of the brain, removal of its encephalograms and a number of other diagnostic techniques, the researchers processed data from 26 elderly people for several months. During the experiments, they were instructed to memorize pairs of words, and then recorded the accuracy of memorization. After an eight-hour sleep the next morning, they were asked to repeat the remembered pairs of words, while simultaneously recording with the help of functional magnetic resonance imaging the activity of the hippocampus, responsible for short-term storage of memories, and the prefrontal cortex, responsible for long-term storage.
The researchers then injected the subjects with a radioactively labeled analogue of the fluorescent dye thioflavin T, known as Pittsburgh compound B. Due to its chemical properties, it selectively binds only beta-amyloids, actively accumulating in the area of their highest concentration. Due to its weak radioactivity, it is easy to distinguish it using positron emission tomography, and therefore the method discovered more than 13 years ago is currently the only way to visualize clusters of amyloid proteins in the human brain. It turned out that in the prefrontal cortex of those who demonstrated deeper sleep and better memory, there was a minimum of beta-amyloids. And their peers, who did not show deep sleep and remembered phrases worse, had beta-amyloids, on the contrary, significantly more than the norm.
On the right is a brain saturated with beta–amyloid proteins (highlighted in red), whose presence is characteristic of people with a lack of deep sleep and an encephalogram showing this deficiency, on the left is a healthy brain with its characteristic encephalogram.
After repeating the experiment many times and analyzing its statistics with the help of specialized software, scientists came to the conclusion that there is a positive feedback between poor sleep and the accumulation of beta-amyloids. Appearing in the prefrontal cortex in significant quantities, they begin to prevent the brain from entering the deep sleep phase, which in turn further accelerates the accumulation of beta-amyloids. Along the way, beta-amyloids somehow, not yet completely clear, prevented the transfer of short-term memories from the hippocampus to the prefrontal cortex, where long-term memories are stored.
The reasons for such an increased accumulation of these proteins, the researchers suggest, may be similar to those previously observed by other groups in the brains of mice. Then it was possible to see how in the phase of deep sleep the brain cells were slightly "compressed", allowing the cerebrospinal fluid to penetrate between them and remove potentially toxic substances, including proteins such as beta-amyloids. In the absence of deep sleep, beta-amyloids were not removed.
Currently, scientists are preparing a new series of experiments in which they will try to determine which of these two factors begins to act first: whether the appearance of beta-amyloids undermines healthy sleep and provokes further accumulation of these substances, which potentially threatens Alzheimer's disease, or failures in sleep mode lead to the appearance of beta-amyloids, provoking subsequent processes.
In any case, the authors of the work note, it is already clear that medicine may well try to break this vicious circle. In addition to drugs for sleep normalization, there are already proven methods of weak electrical stimulation of the brain that can increase the depth of sleep and thus potentially suitable for breaking the positive feedback "deep sleep deficiency – accumulation of beta-amyloids".
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