- A hormone called irisin released during training reduces plaques in the brain
- It causes higher levels of the enzyme neprilysin, which removes beta amyloid.
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The reason why exercise can prevent Alzheimer’s disease has been discovered and could lead to new treatments for this incurable disease.
Experts have shown that a hormone called irisin that is released during exercise removes plaques in the brain associated with the memory-robbing condition.
In a laboratory study, amyloid beta proteins exposed to irisin showed a “marked reduction.”
Physical exercise has been shown to reduce amyloid beta deposits in several mouse models, but the mechanisms involved remain a mystery.
Now the study, published in the journal Neuronsolves the puzzle and promises new ways to prevent or cure the condition.
Experts have discovered that a hormone called irisin that is released during exercise reduces the plaques and tangles in the brain that are thought to cause Alzheimer’s.
For example, researchers said it could boost potential new treatments, such as irisin injected into the bloodstream.
Senior author of the study, Dr. Se Hoon Choi, assistant professor of neurology at Massachusetts General Hospital (MGH), said: “First, we found that irisin treatment led to a notable reduction in amyloid beta pathology. .
“Second, we showed that this effect of irisin was attributable to increased neprilysin activity due to increased levels of neprilysin secreted by brain cells called astrocytes.”
The team had previously developed the first 3D model of Alzheimer’s disease: a system of cells built in a laboratory to represent a human brain with this disease.
He had the two main hallmarks of the condition: beta amyloid deposits and tau tangles in the brain.
It was already known that exercise causes muscles to release irisin, thus increasing levels in the body.
Improves muscle activity, increasing the amount of energy that muscles can use.
The team applied the hormone to their 3D model of a human brain with Alzheimer’s disease.
Neprilysin is an enzyme that breaks down amyloid beta found in the brains of mice that were given exercise.
Previous studies have shown that in mice, irisin injected into the bloodstream can reach the brain, making it potentially useful as a therapeutic.
Dr. Rudolph Tanzi, lead author of the study and director of the Genetics and Aging Research Unit at MGH, said: “Our findings indicate that irisin is an important mediator of exercise-induced increases in neprilysin levels, leading to a reduction in amyloid beta load, suggesting a new target pathway for therapies aimed at the prevention and treatment of Alzheimer’s disease.’
