The reason exercise can prevent Alzheimer’s disease has been discovered and could lead to new treatments for the incurable 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.
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.
The team from Massachusetts General Hospital had previously developed the first 3D human cell culture models of Alzheimer’s.
This displayed two major hallmarks of the condition, the generation of amyloid beta deposits followed by tau tangles in the brain.
It was known that exercise increases circulating levels of the muscle-derived hormone irisin, which regulates glucose and lipid metabolism in fat tissue and increases energy expenditure by accelerating the browning of white fat tissue.
Previous studies have revealed that irisin occurs in human and mouse brains but is reduced in those 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.
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 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.”
