12 February 2019

Running from dementia

The hormone irisin will help to "escape" from dementia and Alzheimer's disease

Maria Perepechaeva, "First-hand Science"

Life expectancy is increasing – this is a plus; a minus is that today tens of millions of people in the world suffer from senile dementia. One of the common causes of dementia is Alzheimer's disease: with this neurodegenerative disease, the hippocampus, the area of the brain responsible for learning and memory processes, primarily suffers. The search for effective drugs that can, if not cure, then at least stop the development of pathology has not yet yielded results, although researchers do not lose hope. 

Today we know that high physical activity helps to improve memory and even reduce the risk of developing Alzheimer's disease. There are suggestions that in this case, the benefits of exercise are due to improved cerebral blood flow, but it seems that everything is not so simple.

A few years ago, it was discovered that during physical activity, a peptide hormone is released into the blood, which plays a role in energy metabolism. This regulatory peptide, named irisin (irisin) in honor of the Greek goddess-messenger of Iris, was even supposed to be used to solve the problem of overweight in humans. Later it turned out that irisin can also stimulate the growth of neurons in the hippocampus, mediating the link between physical activity and improved cognitive abilities.

Now scientists from Brazil, the USA and Canada have studied the relationship between the level of irisin in brain tissues and symptoms characteristic of Alzheimer's disease.

Article by Lourenco et al. Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer's models published in the journal Nature Medicine. A press release on How Exercise May Protect Against Alzheimer's is available on the Columbia University website.

Brain tissue samples from healthy and sick people, as well as laboratory mice – both healthy and "models" of Alzheimer's disease - were used for research. In some animals, the tendency to this pathology was genetically programmed, in others it was imitated by injections into the brain of a pathological beta-amyloid protein that accumulates in Alzheimer's disease. Irisin was found in samples of both human and mouse hippocampus, while its level was higher in samples of healthy tissues.

Then the scientists "turned off" the gene encoding irisin in the brains of healthy mice, which led to a deterioration in memory indicators in behavioral tests, as well as a decrease in synaptic plasticity in animals, which is the physical basis of memory and learning processes. Conversely, injecting irisin into the brains of Alzheimer's model mice improved all these indicators.

The researchers then studied the effect of exercise on cognitive performance in animals that were injected with a pathological protein into the brain. In mice that were forced to swim (for an hour a day, five days a week for five weeks), memory did not deteriorate, unlike their companions, who were constantly sitting in cages. But if the swimmer mice were injected with an irisin blocker, then no positive effect from the classes was observed.

The leitmotif of this work is clear: you need to do physical education. But taking into account age-related diseases, not all elderly people can afford it. Therefore, of course, it is necessary to develop drugs that can either increase the level of irisin in the brain, or simulate its effect. And now researchers are actively looking for them.

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