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Keep Your Memory Sharp With Exercise

A fascinating new research demonstrates how exercise may improve brain health. A hormone generated by muscles during exercise may pass into the brain and improve the health and function of neurons, boosting thinking and memory in both healthy mice and those with a rodent form of Alzheimer’s disease, according to the research. People generate the same hormone during exercise, according to previous study, and the findings imply that movement might change the course of memory loss in old age and dementia.

We already have plenty of evidence that exercise is beneficial to the brain. Exercise promotes the production of new neurons in the brain’s memory region, which then helps those new cells survive, mature, and integrate into the brain’s neural network, where they can aid in thinking and remembering, according to studies in both people and animals. Active people are also less likely to acquire Alzheimer’s disease and other types of dementia than those who rarely exercise, according to large-scale epidemiological research.

But, on a molecular level, how does exercise alter the inner workings of our brains? Exercise, without engaging muscles, might affect the molecular milieu within the brain, according to scientists. Alternatively, during physical exercise, muscles and other tissues may produce chemicals that go to the brain and kick-start processes there, resulting in improved brain health. However, the chemicals would have to be able to pass across the blood-brain barrier, which protects our brains from the rest of our bodies and is generally impenetrable.

A big group of experts from Harvard Medical School and other institutions were particularly interested in these complex difficulties a decade ago. In 2012, a team of scientists led by Bruce M. Spiegelman, the Stanley J. Korsmeyer Professor of Cell Biology and Medicine at the Dana-Farber Cancer Institute and Harvard Medical School, discovered a previously unknown hormone that is produced in the muscles of lab rodents and people during exercise and then released into the bloodstream. The novel hormone was given the name irisin after the Greek messenger deity Iris.

When researchers followed the path of irisin in the circulation, they discovered that it frequently landed on fat tissue, where it was sucked up by fat cells, triggering a chain of metabolic events that led to the transformation of regular white fat into brown fat. Brown fat is significantly more metabolically active than white fat, which is far more prevalent. It consumes a lot of calories. As a result, by assisting in the formation of brown fat, irisin aids in the acceleration of our metabolism.

However, Spiegelman and his colleagues hypothesized that irisin may have a function in brain health as well. Irisin is generated in the brains of mice after exercise, according to a 2019 study by other researchers. The hormone was also found in the majority of human brains donated to a big brain bank, unless the donors had died of Alzheimer’s disease, in which case their brains had almost little irisin.

Irisin appears to reduce the risk of dementia, according to that study. Spiegelman and his partners, including Christiane D. Wrann, an assistant professor at Massachusetts General Hospital and Harvard Medical School and a senior author of the current study, set out to quantify how in a new study published last week in Nature Metabolism.

They started by breeding mice that were born unable to make irisin and then allowed those mice, as well as other adult mice, to run about on wheels for a few days, which the animals seemed to enjoy. This type of activity generally improves future performance on memory and learning tests in rodents, as shown in the regular runners. The rats that were unable to produce irisin, on the other hand, exhibited no cognitive gain, leading the researchers to infer that irisin is required for exercise to improve thinking.

They next examined the brains of running mice with and without the ability to produce irisin in more detail. All of them had more newborn neurons than sedentary mice’s brains. Those new brain cells seemed strange in the animals who did not have irisin. They had fewer synapses, the connections between brain cells where signals are sent and received, and dendrites, the snaky tendrils that connect neurons to the neural communications system. The researchers determined that these newly generated neurons would not simply integrate into the brain’s existing network.

However, when scientists employed drugs to boost irisin levels in the blood of animals who couldn’t generate it on their own, the situation in their brains drastically changed. Young mice, old mice, and even those with advanced instances of mouse Alzheimer’s disease began to perform better on memory and learning tasks. The researchers also discovered indications of decreased inflammation in the brains of dementia-affected rats, which is significant since neuroinflammation is considered to expedite memory loss development.

They also confirmed that irisin reaches the blood-brain barrier and passes it. The hormone appeared in the brains of the genetically engineered mice when the researchers injected it into their bloodstreams, despite the fact that their brains could not have created it.

These new studies, taken together, clearly show that irisin is a significant factor in “linking exercise to cognition,” according to Spiegelman.

It may possibly be developed as a medicine in the future. Spiegelman and his colleagues aim to explore if pharmaceutical versions of irisin might delay cognitive loss or possibly improve thinking skills in Alzheimer’s patients in the future.

However, this was a mouse study, and further research is needed to determine if our brains react to irisin in the same way as rodents’ do. It’s also unclear how much or what sorts of activity will boost our irisin levels the most. However, Wrann believes that the study confirms that exercise is “one of the most significant regulators” of brain health.

 

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