The reason exercise can prevent Alzheimer’s disease has been discovered and could lead to new treatments for the incurable condition.
Experts have shown that a hormone called irisin released during a workout clears plaques in the brain associated with the memory-robbing condition.
In a study in a lab, amyloid beta proteins exposed to irisin showed ‘remarkable reduction.’
Physical exercise has been shown to reduce amyloid beta deposits in various mouse models, but the mechanisms involved have remained a mystery.
Now the study, published in the journal Neuron, solves the puzzle and promises new ways to prevent or cure the condition.
Experts have found that a hormone called irisin released during a workout reduces the plaques and tangles in the brain thought to cause Alzheimer’s
For example, the researchers said it could spur new potential treatments, such as irisin injected into the bloodstream.
Lead 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 remarkable reduction of amyloid beta pathology.
‘Second, we showed this effect of irisin was attributable to increased neprilysin activity owing to increased levels of neprilysin secreted from cells in the brain called astrocytes.’
The team had previously developed the first 3D model of Alzheimer’s — a system of cells built in a lab to represent a human brain with the condition.
It had the two major hallmarks of the condition — amyloid beta deposits and tau tangles in the brain.
It was already known that exercise causes muscles to release irisin, therefore increasing levels in the body.
It improves muscle activity, increasing the amount of energy muscles can use.
The team applied the hormone to their 3D model of a human brain of Alzheimer’s disease.
Neprilysin is an amyloid beta–degrading enzyme found in the brains of mice who were made to exercise.
Previous studies have shown that in mice, irisin injected into the bloodstream can make its way into the brain, making it potentially useful as a therapeutic.
Dr Rudolph Tanzi, a senior author of the study and director of the Genetics and Aging Research Unit at MGH, said: ‘Our findings indicate that irisin is a major mediator of exercise-induced increases in neprilysin levels leading to reduced amyloid beta burden, suggesting a new target pathway for therapies aimed at the prevention and treatment of Alzheimer’s disease.’
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