Exercise’s secret for preventing Alzheimer’s disease discovered by scientists

BOSTON — Why does breaking a sweat lead to better brain health? Researchers in Boston may finally have an answer. A new study has discovered why exercise may prevent Alzheimer’s disease, potentially paving the way for new treatments for the currently incurable condition.

Experts at Massachusetts General Hospital found that during exercise, the body releases a hormone called irisin. This hormone has been shown to reduce the brain plaques and tangles commonly associated with Alzheimer’s disease onset.

While physical exercise has consistently demonstrated its ability to reduce amyloid beta deposits in mouse experiments, the exact mechanisms remained unclear until now. The study, published in the journal Neuron, clears up this mystery and also suggests potential avenues for prevention and treatment of Alzheimer’s — the most common form of dementia.

The Mass General team pioneered the development of the first 3D human cell culture models for Alzheimer’s. These models showcase two primary characteristics of the disease: the formation of amyloid beta deposits and subsequent tau tangles in the brain.

Older man wiping off the sweat from an intense exercise workout at the gym.
(Photo by Mladen Zivkovic on Shutterstock)

It’s well-documented that exercise elevates the levels of the muscle-derived hormone irisin, which not only helps regulate glucose and lipid metabolism in fat tissues but also enhances energy expenditure by promoting the conversion of white fat into brown fat. Earlier research indicated that irisin is present in both human and mouse brains. However, its levels are diminished in individuals with Alzheimer’s. With this knowledge, the research team introduced irisin to their 3D cell culture model of Alzheimer’s.

“First, we found that irisin treatment led to a remarkable reduction of amyloid beta pathology,” says Dr. Se Hoon Choi in a media release. “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.”

Notably, neprilysin — an enzyme that degrades amyloid beta — has been identified in the brains of exercise-exposed mice. Previous studies have also demonstrated that when irisin is injected into the bloodstream of mice, it can permeate the brain, indicating its potential therapeutic utility.

“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,” says Rudolph Tanzi, PhD, a senior author of the study and director of the Genetics and Aging Research Unit.

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South West News Service writer Jim Leffman contributed to this report.

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