Exercise-Induced Hormone Irisin May Reduce Alzheimer’s Disease Plaque and Tangle Pathology in the Brain, suggesting new therapeutic strategies for the treatment of Alzheimer’s disease

Key Takeaways

• Researchers have used a 3D human neural cell culture model to show that the exercise-induced muscle hormone, irisin, reduces the level of amyloid beta associated with Alzheimer’s disease

• Irisin had this effect by triggering brain cells called astrocytes to increase production of the amyloid beta–degrading enzyme neprilysin

• The findings could lead to new therapeutic strategies for the treatment of Alzheimer’s disease

Summary

• Researchers at Massachusetts General Hospital (MGH) have found that irisin, a hormone produced by muscle cells, can help reduce amyloid beta deposits in the brain, a hallmark of Alzheimer's disease (AD).

• The study, published in the journal Neuron, used a 3D human cell culture model of AD to show that irisin treatment led to a significant reduction in amyloid beta pathology.

• The researchers also found that irisin's ability to reduce amyloid beta was due to its ability to increase the activity of neprilysin, an enzyme that breaks down amyloid beta.

• Additionally, the researchers identified integrin αV/β5 as the receptor on astrocytes that irisin binds to in order to increase neprilysin activity.

• This finding suggests that irisin could be a potential therapeutic target for AD.

The study's findings are significant because they provide new insights into the role of irisin in AD and suggest that it could be a potential therapeutic target for the disease.

Additional Details

• Physical exercise has been shown to reduce amyloid beta deposits in mouse models of AD, but the mechanisms involved have remained a mystery.

• 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.

• Studies have shown that irisin is present in the brains of humans and mice, and that its levels are reduced in patients with AD and in mouse models of the condition.