How Exercise Helps Fight Alzheimer’s Disease

by Ravi Ram

Alzheimer’s disease is a devastating condition that affects millions of people worldwide. With no cure or effective treatment currently available, researchers are tirelessly working to unravel the mysteries of this disease and find new avenues for intervention. In a recent study published in the journal Neuron, scientists from Massachusetts General Hospital (MGH) have made a significant breakthrough by identifying a protein called irisin that can break down amyloid beta in the brain.

Amyloid beta is a protein fragment that clumps together to form plaques in the brains of Alzheimer’s patients. These plaques obstruct important signaling pathways and impair memory formation. Scientists have long suspected that physical activity and exercise can reduce amyloid beta buildup in the brain and improve cognitive health, but the underlying mechanisms have remained unclear.

Irisin is a hormone released by muscles during exercise that regulates glucose and fat metabolism. It also converts white fat tissue into brown fat tissue, improving energy expenditure. In the study, the researchers created a three-dimensional model of Alzheimer’s disease to simulate the brain’s architecture more accurately. They found that exposure to irisin significantly reduced amyloid beta deposits in the model, suggesting a direct link between the hormone and improved cognitive function.

Further experiments revealed that irisin binds to astrocytes, cells in the brain that provide support and essential functions for neurons. These astrocytes secrete an enzyme called neprilysin, which degrades amyloid beta and improves memory function in mice with Alzheimer’s disease. When irisin binds to astrocytes, it triggers an increase in neprilysin production, leading to a decrease in amyloid beta deposits.

The researchers also identified the surface receptor on astrocytes that allows irisin to bind effectively. Additionally, they discovered that irisin downregulates two critical signaling proteins, extracellular signal-regulated kinase (ERK)-signal transducer and activator of transcription 3 (STAT3), to enhance neprilysin levels.

While the findings are promising, it is essential to approach them with caution. Three-dimensional cell-culture models have their limitations and cannot fully replicate the complexity of the human brain. Animal models are also not always reliable in predicting outcomes in humans. Therefore, further research and human trials are necessary to validate these findings.

Nevertheless, the study sheds light on the positive effects of exercise on cognitive health and highlights the role of irisin in reducing amyloid beta buildup. This discovery opens up new possibilities for the development of treatments and preventive strategies for Alzheimer’s disease. Alongside irisin, other proteins like platelet factor 4 and klotho have also been linked to improved cognitive function, emphasizing the importance of physical activity for brain health.

In conclusion, the research conducted by Eunhee Kim and colleagues at MGH provides valuable insights into the mechanisms underlying the cognitive benefits of exercise in Alzheimer’s disease. By understanding how irisin influences amyloid beta deposits, scientists can explore new avenues for intervention and potentially improve the lives of millions affected by this silent pandemic.

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