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Muscle-Brain Crosstalk: How Skeletal Muscle Influences Neurocognitive Function
Sarcopenia, commonly associated with the frailty of advanced age, goes beyond mere muscle weakness—it holds potential implications for our cognitive faculties. But what links the muscle's decline to the brain's? The answer, it seems, could lie in the realm of myokines—specific chemicals our muscles dispatch during exercise, intricately connected to brain health. Factor in disturbances like insulin imbalances, protein metabolism anomalies, compromised mitochondrial functions, mounting inflammation, and a portrait of cognitive erosion emerges. In their recent review, Oudbier et al. dissect these connections. In this research review, we dive into their analysis, revealing the biochemical and physiological connections between skeletal muscle and the brain, and the pathophysiological mechanisms underlying cognitive decline.
Central to their findings are four pivotal mechanisms potentially bridging muscle deterioration with cognitive aging: the domino effects of systemic inflammation, insulin resistance, abnormal protein accumulation, and mitochondrial dysfunction. But certain molecular mechanisms offer compelling links between the two, such as changes in the secretion of muscle-specific chemicals (myokines), inflammation, insulin issues, protein accumulation anomalies, oxidative stress, and, not surprisingly, problems in our cellular powerhouses, the mitochondria (24). This process of oxidative stress has been identified as a common mechanism underlying two distinct age-related conditions: sarcopenia, which involves a decrease in skeletal muscle mass and function, and dementia, which encompasses various cognitive impairments.
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