Sleep is no longer considered only a period of relaxation, but rather a necessary vital process during which nerve cells carry out precise repairs at the energy and metabolic levels. This conclusion is supported by recent research that focuses on studying sleep from a cellular and molecular perspective, rather than exclusively behavioral analyses.
Scientist Amita Sehgal, professor of molecular biology at the University of Pennsylvania, explains that sleep is a universal phenomenon shared by most living organisms, which indicates the existence of a basic function and a common goal behind this process.
Her research team’s results indicate that there is a close link between sleep and the process of energy production within neurons, specifically the function of mitochondria, which serve as the cell’s power plants.
During periods of wakefulness, neurons work with intense activity, producing oxidative molecules that may cause damage to mitochondria and the cells themselves.
The study shows that sleep helps transport oxidized fats resulting from this activity from neurons to supporting glial cells, where they are broken down or eliminated. This mechanism is believed to contribute to protecting neurons and maintaining their efficiency.
Researchers have also linked sleep to autophagy, a cellular mechanism for recycling damaged components, including damaged mitochondria. The results indicate that these processes are most active during sleep, strengthening the hypothesis that the brain uses this period to carry out maintenance tasks that cannot be accomplished with the same efficiency while awake.
The study also examined the possible relationship between sleep disorders and neurodegenerative diseases such as Alzheimer’s. Some of the cellular pathways regulated by sleep, such as fat metabolism and autophagy, are the same as those affected in Alzheimer’s disease. The researchers also highlighted the role of the APOE protein, which is linked to an increased risk of disease, in transporting fats between nerve cells.
