Postmenopausal Sarcopenia And Alzheimer’S Disease: The Interplay Of Mitochondria, Insulin Resistance, And Myokines

The paper suggests that the decline in muscle mass after menopause, known as sarcopenia, may contribute to the development of Alzheimer’s disease through complex interactions involving cellular energy production, the body’s ability to regulate blood sugar, and signaling molecules released by muscles.

As women age, particularly after menopause, many experience a natural decline in muscle mass, a condition called sarcopenia. This isn’t just about physical strength; new research explores how this muscle loss might be connected to an increased risk of developing Alzheimer’s disease, a condition that affects memory and thinking. The connection appears to involve several key biological processes. One crucial factor is the health of our mitochondria, often called the “powerhouses” of our cells, which are responsible for generating energy. When these don’t function properly, it can impact both muscle and brain health. Another important link is insulin resistance, where the body’s cells don’t respond effectively to insulin, leading to higher blood sugar levels. This is known to affect brain health and is often seen in both sarcopenia and Alzheimer’s. Finally, muscles release special signaling molecules called myokines. These myokines can travel throughout the body and influence other organs, including the brain. Changes in the types and amounts of myokines released by aging muscles might play a role in the communication between muscles and the brain, potentially influencing the risk of neurodegenerative diseases like Alzheimer’s. Understanding these intricate connections could open new avenues for preventing or treating Alzheimer’s disease by focusing on muscle health.

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Source: link to paper