How exercise can help keep our memory alive

A new study reveals that a hormone released during exercise can improve brain health and lessen the damage and memory loss that occur during dementia.

The study, published this month in Nature Medicine, involved mice, but its findings could help explain how, at the molecular level, exercise protects our brain and possibly preserves memory and thinking abilities even among people whose past fades.

Numerous scientific evidence already demonstrates that exercise reshapes the brain and affects thinking.

Researchers have shown in rats and mice that running accelerates the creation of new brain cells in the hippocampus, a part of the brain devoted to training and storing memory.

Exercise can also improve the health and function of synapses between neurons, allowing brain cells to communicate better.

Epidemiological research in humans indicates that being physically active reduces the risk of Alzheimer's disease and other dementias and can also slow the progression of the disease.

But many questions remain about how exercise alters the inner workings of the brain and whether the effects result from changes elsewhere in the body that are also good for the brain or if the changes actually occur in the brain itself. -even.

These questions attracted the attention of an international consortium of scientists, some neuroscientists, and other cell biologists, all dedicated to the prevention, treatment and understanding of Alzheimer's disease.

These concerns had brought a hormone called irisine into their sphere of interest.

Irisin, identified for the first time in 2012 and named for Iris, the messenger of the gods in Greek mythology, is produced by the muscles during exercise.

The hormone triggers multiple biochemical reactions throughout the body, most of them related to energy metabolism.

Since Alzheimer's disease is thought to involve, in part, changes in brain energy use, scientists believe that exercise can help protect the brain by increasing irisin levels. in the brain.

But if that was the case, they realized that irisin should exist in the human brain. To see if this was the case, they took tissue from brain banks and, using sophisticated tests, found irisin.

Patterns of gene expression in these tissues also suggested that much of this irisin had been created in the brain itself.

Hormone levels were especially high in the brains of people who did not have dementia at the time of their death, but were barely detectable in the brains of people who died with Alzheimer's disease .

These tests, although interesting, have not allowed scientists to determine the role that irisin might play in the brain. The researchers turned to mice, some healthy and others raised to develop a form of rodent Alzheimer.

They infused a concentrated dose of irisin into the brain of animals destined for dementia. These mice quickly began to perform better in memory tests and to show signs of improvement in synaptic health.

At the same time, they soaked the brain of healthy animals with a substance that inhibits irisin production, and then injected a form of beta-amyloid, a protein that agglomerates to form plaques in people's brains with Alzheimer's disease. Indeed, they caused dementia in mice.

And, without any irisin in their brains, the once healthy mice quickly showed signs of memory worsening and synaptic dysfunction between the neurons of their hippocampus.

Scientists also examined the interior neurons of healthy mice and found that, when they added irisin to the cells, gene expression was altered to reduce the damage caused by beta-amyloid.

Finally and perhaps most importantly, the scientists worked healthy mice, swimming for one hour almost every day for five weeks.

Previously, some animals were also treated with the substance that blocks the production of irisin.

In untreated animals, levels of irisin in the brain flourished during exercise. Later, after the brain's exposure of these animals to beta-amyloid, they seemed to combat the effects, which gave better results to memory tests than sedentary control mice were exposed.

But animals unable to create irisin did not benefit much from exercise. After being exposed to beta amyloid, they have been about as unsuccessful in memory tests as sedentary animals with beta-amyloid in the brain.

Taken together, these experiments suggest that exercise can protect against dementia by increasing the amount of irisin in the brain, says Ottavio Arancio, professor of pathology and cell biology at Columbia University, who led the study. research with two dozen colleagues from the Federal University of Rio de Janeiro in Brazil, Queen's University in Canada and other institutions.

But the experiments, although elaborate and themed, used mice and could not tell us if exercise and irisine would work in the same way in humans, or what type and what type of exercise would be the best for brain health.

The results also do not show whether exercise and irisine can prevent Alzheimer's disease, but only that they seem to lessen some of the effects of the disease in the mouse once it has started.

The scientists involved in the study are hoping to soon test a pharmaceutical form of irisine as a treatment for dementia in animals and, possibly, in people, particularly those who have lost the ability to do so. exercise, says Arancio.

But for the moment, he says, the main lesson of the study seems to be that "if you can, go for a walk".