Alzheimer's: experts figure out why exercise can help prevent the progressive condition

It's all due to a hormone which increases when exercising

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Experts have discovered the reason why exercise can help prevent Alzheimer’s disease.

During exercise, a hormone called irisin is released which reduces the plaques and tangles in the brain thought to cause Alzheimer’s.

It is known that physical exercise reduces amyloid beta deposits in various mouse models, but researchers did not know why.

Runners jog along Kite Beach (Image: Warren Little/Getty Images)Runners jog along Kite Beach (Image: Warren Little/Getty Images)
Runners jog along Kite Beach (Image: Warren Little/Getty Images)

In the journal Neuron, a team of researchers from Massachusetts General Hospital had previously developed the first 3D human cell culture models of Alzheimer’s.

The model displayed two major hallmarks of the condition: the generation of amyloid beta deposits followed by tau tangles in the brain.

The muscle-derived hormone irisin increases when people exercise. Irisin regulates glucose and lipid metabolism in fat tissue and increases energy expenditure by accelerating the browning of white fat tissue.

Previous studies show that irisin is reduced in mice suffering from Alzheimer’s.

So the team applied the hormone to their 3D cell culture model of Alzheimer’s disease.

Dr Se Hoon Choi 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.”

Neprilysin is an amyloid beta–degrading enzyme found in the brains of mice exposed to exercise.

In mice, when irisin is 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 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.”