Why do we need to sleep? What is the biological mechanism that triggers fatigue, a feature that unites all organisms with a nervous system, including flies, jellyfish and worms? New research from the Israeli University of Bar Ilan provides some pieces towards the solution of one of the still unsolved evolutionary puzzles.
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“Sleeping is a strange thing,” he says to Salute the professor Lior Appelbaum, who drives, together with Dr. David Zada, the team of researchers who published the study in the scientific journal in November Molecular Cell. “It may seem counterintuitive with respect to the mechanisms of evolution because it means entering a condition of vulnerability: there are those who die from it. A little fish falls asleep and is swallowed by a shark. Yet, it is evidently a very important mechanism since all animals sleep “.
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Appelbaum and Zada’s study for the first time provides an answer on the mechanism that causes fatigue by forcing the body to stop. During the waking hours, innumerable DNA damages accumulate inside the nerve cells (neurons), caused by various factors, including the activity of the cells, exposure to UV rays, enzymatic errors. After many hours of operation, the DNA is comparable to a highway full of potholes, which needs to be repaired, explains Appelbaum.
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And what is the best time, if not at night, when there is less traffic and movement? In simple terms, this is what happens while we sleep: neurons use the hours of sleep to repair the DNA that is in their nucleus. The fatigue mechanism is activated to push the body to stop its activity, allowing the process of “maintenance” of our genetic chain to be more effective.
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The researchers proved their point through a series of experiments on zebrafish and partly on rodents as well. “Fish have characteristics very similar to humans and vertebrates in general. But the main factor is that zebrafish, when they are small, are transparent and this allows us to examine all the processes under a microscope without having to make any incisions”, Appelbaum explains. In one of the experiments, the researchers genetically engineered the fish, coloring the proteins responsible for the repair system inside the cell. In this way, they were able to verify that, during the waking hours, the proteins are scattered in different points within the cell, while during sleep they are concentrated in the damaged areas.
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Another experiment specifically concerns the repairing protein PARP1, one of the first to respond to DNA damage and identified as responsible for the fatigue effect. “When we increased PARP1 in the cell, the fish fell asleep, when we inhibited it, it stayed awake, was unaware of its fatigue and the damage was not repaired regularly.”
On the basis of these findings, can we therefore think that one day it will be possible to control the amount of hours of sleep that each of us needs? Here we are still in the realm of speculation, but Appelbaum’s article sets the theoretical assumptions for the possibility of measuring the amount of damage that accumulates in the DNA and, consequently, of predicting the hours of sleep necessary to repair it.
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The research also confirms what in our daily life is a rather established convention, namely that an average of six consecutive hours seems to be a good compromise of hours of rest for the body. At least that’s the case with zebrafish too. “Fish are very sensitive to light. In the experiments we gradually reduced the hours of darkness. If we gave them only two, for example, we found that they continued to sleep, despite the light, for up to six hours, which is exactly the minimum of. hours of sleep also required in the military, “Applebaum says.
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PARP1 also plays an important role in oncological treatments. The same inhibitory material used by the researchers to decrease the amounts of the repair protein in their experiments on zebrafish is in fact used in chemotherapy (to prevent the protein from “repairing” the malignant cell that the treatment wants to eliminate). Reason why chemotherapy causes great tiredness and sleep disturbances to those who are subjected to it. While this was not the focus of the research, applied only to neurons, Appelbaum’s lab demonstrated the connection between lack of sleep and neurodegenerative diseases such as Parkinson’s or Alzheimer’s. Insights into sleep function in nerve cell repair mechanisms could provide a breakthrough in the study of a cure for these diseases. This is one of the future challenges of the Bar Ilan University team, in addition to experimenting with research in as many organisms, from invertebrates to humans.
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