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A recent study in Boston reveals that exercise can improve brain health and possibly help prevent Alzheimer’s disease. This breakthrough could lead to potential treatments for the currently untreatable condition.

Exercise triggers release of irisin hormone lowering brain plaques

Researchers from Massachusetts General Hospital have discovered that exercise triggers the release of a hormone called irisin. This hormone has demonstrated the ability to lower the brain plaques and tangles linked to the onset of Alzheimer’s disease.

Physical exercise has been shown to reduce deposits of amyloid beta in mouse studies. A recent study in the journal Neuron explains the underlying mechanisms and hints at possible Alzheimer’s prevention and treatment strategies.

Exercise is known to increase the muscle-derived hormone irisin, regulating glucose and lipid metabolism in fat tissues and converting white fat into brown fat to boost energy expenditure. Previous studies showed irisin in human and mouse brains, but it’s reduced in Alzheimer’s patients. Researchers added irisin to an Alzheimer’s 3D cell culture model to investigate its potential effects.

Dr. Se Hoon Choi said that the research revealed that irisin treatment significantly reduced amyloid beta pathology, primarily due to the enhanced neprilysin activity. This effect was linked to increased neprilysin secretion from brain cells known as astrocytes.

Mice engaging in exercise have high levels of neprilysin

Significantly, neprilysin, an enzyme responsible for breaking down amyloid beta, has been detected within the brains of mice exposed to physical activity. Earlier research has also illustrated that the introduction of irisin into the circulatory system of mice allows it to penetrate the brain, suggesting its potential value as a therapeutic agent.

According to Dr. Rudolph Tanzi, the senior author of the research and the director of the Genetics and Aging Research Unit, the results suggest that irisin plays a significant role in the elevation of neprilysin levels triggered by exercise. This, in turn, results in a reduction in amyloid beta accumulation. These findings point towards a novel therapeutic pathway for addressing Alzheimer’s disease, offering potential strategies for both prevention and treatment.