Scientists discover a protein whose deficiency leads to neurodegenerative diseases

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Scientists at the Skolkovo Institute of Science and Technology have discovered that the nuclear protein sirtuin-6 plays a role in protecting DNA from damage, in fat and glucose metabolism and many other important processes, as well as in the energy of the cell without it. supply breaks down. This was reported to socialbites.ca by the Russian Science Foundation, which supported the work with a grant.

According to the authors, the protein functions as a central regulator of the activity of cellular “energy stations” – mitochondria – in the brain. When there is a disruption in the operation of these “energy stations”, the person develops neurodegenerative diseases, for example, Alzheimer’s or Parkinson’s disease.

“Our results clearly show that a decrease in sirtuin-6 level in the brain of the elderly may be almost the main cause of age-related neurodegenerative diseases. Now we have to look at the details: why is this happening? Project manager Ekaterina Khrameyeva now hypothesizes that everything can be attributed to DNA packaging,” project manager Ekaterina Khrameyeva told socialbites.ca. “We’re trying to test it because sirtuin-6 separates a group of atoms from the DNA “packers” and thus controls its folding and unfolding,” he said.

The researchers conducted an experiment with mice that had their sirtuin-6 reduced. To understand exactly which genes are working in neurons, biologists isolated RNA from the brains of animals and deciphered its sequence. The scientists also analyzed the amount of substances associated with mitochondrial activity.

The results of the study showed that sirtuin-6 deficiency leads to pathological changes. That is, about 3,000 genes were affected, and especially those associated with mitochondria. The authors noted a direct link between sirtuin-6 deficiency and mitochondrial death – with a 20% reduction in protein levels, the mice had approximately the same number of these organelles in their brain cells.

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