Khaberni - A recent scientific study revealed that lack of sleep not only causes feelings of fatigue and mental sluggishness but directly damages the delicate structure of the brain.
According to research published in the journal "Proceedings of the National Academy of Sciences," sleep deprivation negatively affects the protective fatty layer surrounding the nerve cells, slowing down the transmission of nerve signals within the brain.
Sleep loss is a common experience most people undergo, and its effects are often associated with feelings of sleepiness and reduced concentration and slow reaction times the following day. Despite the prevalence of these symptoms, the underlying biological mechanisms were not fully understood, as it was long believed they were only due to the fatigue of the nerve cells.
However, a research team led by scientists from the University of Camerino in Italy hypothesized the existence of other factors and decided to delve deeper into finding the real cause.
The researchers relied on analyzing MRI images of 185 volunteers who reported poor sleep quality, and the results confirmed a link between sleep deprivation and changes in the white matter structure of the brain, responsible for transmitting signals between nerve cells.
To understand the direct cause, the team conducted experiments on mice deprived of sleep for ten days. Electrical tests showed that nerve signals took about 33% longer to travel between the halves of the brain, compared to normal conditions.
Upon examining brain tissues, the researchers found that the layer known as “myelin”—a fatty layer that acts as an insulator speeding up the nerve signal transmission—had become much thinner.
Molecular analyses showed that the primary cause was due to a malfunction in regulating cholesterol within cells known as “oligodendrocytes,” which are responsible for the production and maintenance of myelin. Cholesterol is essential for maintaining the thickness of this insulator, but lack of sleep impaired its proper transport, weakening the efficiency of nerve signals.
To test this hypothesis, the researchers used a compound called “cyclodextrin,” which works to release the trapped cholesterol inside the cells and return it to the normal cycle. This intervention successfully prevented the thinning of myelin, eliminated the delay in nerve signal speed, and the mice regained their normal performance in behavioral tests.
Despite the promising results, the researchers emphasized that it is too early to talk about direct treatments for sleep deprivation in humans. However, they pointed out that confirming these results in humans could open the door to new strategies for dealing with the neural effects of sleep deprivation.
The researchers stated in their study: "Our results highlight a potential role for the dysregulation of cholesterol regulation in oligodendrocytes in the behavioral impairment associated with sleep deprivation, revealing a new potential target for therapeutic intervention."
