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Researchers at Lobachevsky University have found new factors that protect the brain from circulatory disorders. Ischemic strokes remain one of the leading causes of death and disability in the world. Many factors are known to disrupt the supply of nutrients and oxygen to the brain cells, and the mechanisms of ischemic damage are similar.

As the most energy consuming organ in the human body, the brain uses up to 20% of all energy and up to 25% of the oxygen the body receives. Even a short-term disruption of cerebral blood flow can have irreversible consequences and cause serious cognitive impairment.

Intracellular signalling mechanisms can protect brain cells from circulatory disorders. However, these mechanisms work differently in different people, which has attracted great interest from researchers and clinicians around the world.

"We studied the molecular mechanisms of brain cell adaptation to oxygen deficiency using three groups of kinase enzymes: Ikkb, Jak2, Flt4. They are involved in the protection of brain cells from hypoxia and have a pronounced therapeutic potential. The regulation of the expression of the genes responsible for the production of these enzymes had an effect not only on cell viability, but also on the neural network activity of the brain both in normal and oxygen-deficient conditions," said project leader Maria Vedunova, Director of the UNN Institute of Biology and Biomedicine.

As a result of their research, scientists at Lobachevsky University have established a pronounced neuroprotective effect of the molecular targets Ikkb and Flt4. The proposed mechanism for dealing with a deficiency of oxygen in brain cells is not related to the commonly known hypoxia-induced factor. It is planned to confirm the new pathway of brain self-protection against oxygen deficiency in the next stage of the in vivo experiment.

Furthermore, the research is aimed at revealing new, previously unknown protective properties of individual representatives of the neuronal kinome in the simulation of ischemic brain damage.

The research was supported by a grant from the Russian Science Foundation (RSF) and interim results were published in the highly ranked journal Oxidative Medicine and Cellular Longevity (journal impact factor 5.392). In 2021, the RSF decided to extend support for the study until June 2023.