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Exercise may keep memory sharp

Studies zoom in on irisin, a hormone released during workouts which may boost brain health and reduce damage from dementia


The Straits Times


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NEW YORK • Exercise control over brain wellness? A hormone released during exercise may improve brain health and lessen the damage and memory loss that occur during dementia, a new study finds.


The study, published this month in Nature Medicine, involved mice, but its findings could help to explain how, at a molecular level, exercise protects people's brains and possibly preserves memory and thinking skills, even in people whose pasts are fading.


Considerable scientific evidence already shows that exercise remodels brains and affects thinking. Researchers have shown in rats and mice that running boosts the creation of brain cells in the hippocampus, a part of the brain devoted to memory formation and storage.


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


In people, epidemiological research shows that being physically active curbs the risk of Alzheimer's disease and other dementias and may slow disease progression.


But many questions remain on just how exercise alters the inner workings of the brain and whether the effects are a result of changes elsewhere in the body that also happen to be good for the brain or whether the changes actually occur within the brain itself.


Those issues attracted the attention of an international consortium of scientists focused on preventing, treating and understanding Alzheimer's disease. Those concerns had brought a hormone called irisin into their sphere of interest.


Irisin, first identified in 2012 and named after Iris, the gods' messenger in Greek mythology, is produced by muscles during exercise. The hormone jump-starts multiple biochemical reactions in the body, most of them related to energy metabolism.


Because Alzheimer's disease is believed to involve, in part, changes in how brain cells use energy, the scientists reasoned that exercise might be helping to protect brains by increasing levels of irisin there.


But if so, they realised, irisin would have to exist in human brains. To see if it did, they gathered tissues from brain banks and, via testing, found irisin there.


Gene expression patterns in the tissues suggested that much of this irisin was created in the brain itself.


Levels of the hormone were especially high in the brains of people free of dementia when they died, but were barely detectable in the brains of people who had died with Alzheimer's.


Those tests, however, though interesting, could not tell scientists what role irisin might be playing in brains. They turned to mice, some healthy and others bred to develop a rodent form of Alzheimer's.


They infused the brains of the animals bred to have dementia with a concentrated dose of irisin. Those mice soon began to perform better on memory tests and show signs of improved synaptic health.


At the same time, they soaked the brains of the healthy mice with a substance that inhibits production of irisin and then pumped in a form of beta amyloid, a protein that clumps together to form plaques in the brains of those with Alzheimer's.


Without any irisin in their brains, the once-healthy mice soon showed signs of worsening memory and poor function in the synapses between neurons in the hippocampus.


The scientists also looked inside individual neurons from healthy mice and found that, when they added irisin to the cells, gene expression changed in ways that would be expected to lessen damage from beta amyloid.


Finally and perhaps most important, the scientists had healthy mice work out, swimming for an hour almost every day for five weeks. Beforehand, some of the animals were also treated with the substance that blocks irisin production.


In the untreated animals, irisin levels in the brain blossomed during the exercise training. Later, after their brains were exposed to beta amyloid, they seemed to fight off its effects, performing much better on memory tests than sedentary control mice that had been exposed.


But the animals that had been unable to create irisin did not benefit much from exercise. After exposure to beta amyloid, they performed about as poorly on memory tests as sedentary animals with beta amyloid in their brains.


Taken as a whole, these experiments suggest that exercise may protect against dementia in part by triggering an increase in the amount of irisin in the brain, said Mr Ottavio Arancio, a professor of pathology and cell biology at Columbia University.


He did the research along with 24 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 multi-pronged, used mice and so cannot tell researchers if exercise and irisin will work similarly in people, or how much and what types of exercise might be best for brain health.


The results also do not show whether exercise and irisin can prevent Alzheimer's, but only that they seem to allay some of the effects of the disease in mice once it begins.


The scientists hope to soon test a pharmaceutical form of irisin as a treatment for dementia in animals and eventually people, especially those who have lost the ability to exercise, Mr Arancio said.


But for now, he said, the big lesson of the study would seem to be that "if you can, go for a walk".




Source: The Straits Times © Singapore Press Holdings Limited. Reproduced with permission.



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