Importance of Maintaining Proteolysis as We Get Older

Proteolysis, the enzymatic breakdown of proteins, is vital for cellular health and function. Its decline is linked to several age-related issues. A primary effect is the loss of muscle mass, or sarcopenia, which occurs as damaged proteins in muscle cells accumulate due to reduced proteolytic activity. This leads to muscle weakness and loss (Source 1, Source 2).

Decreased proteolytic activity also contributes to protein aggregation in neurodegenerative diseases like Alzheimer’s, characterized by the buildup of misfolded proteins. Normally, these proteins are degraded by proteolytic enzymes. A reduction in this activity results in the formation of plaques typical of various neurodegenerative diseases (Source 1, Source 2).

Additionally, impaired cellular function can stem from a reduction in proteolytic activity with age. Proteolysis is crucial for degrading damaged or obsolete proteins, maintaining cellular balance. When this function declines, protein buildup impairs cellular operations, contributing to aging and related diseases (Source 1, Source 2).

Proteolytic activity also impacts atherosclerosis, or arterial plaque formation. Proteolytic enzymes are essential for degrading the arterial wall’s extracellular matrix. A balance disruption in these enzymes can lead to plaque development, arterial thickening, and reduced elasticity, exacerbating atherosclerosis (Source 1, Source 2).

Nattokinase, a proteolytic enzyme, is linked to plaque reversal at high doses and interacts with plasminogen activator inhibitor-1 (PAI-1), influencing longevity. Less PAI-1 production correlates with a 7-year increase in lifespan. Overactivation of PAI-1, which inhibits proteolysis, is common in numerous diseases. Inhibiting PAI-1 can significantly alleviate conditions like fatty liver and dyslipidemia, activate the longevity molecule FGF21 fivefold, and reduce PCSK9 (Source 1, Source 2, Source 3).

Success stories about reversing plaque (CAC score) by lowering LDL levels and using high-dose nattokinase supplements have been reported. Moreover, products like Wobenzym have shown potential in lowering elevated TGF-beta, found to be rejuvenating in mice (Source 1, Source 2).

In conclusion, maintaining robust proteolytic activity is essential for managing age-related conditions such as sarcopenia, neurodegenerative diseases, cellular dysfunction, and atherosclerosis. Targeting molecules like PAI-1 and using proteolytic enzymes like nattokinase might offer viable therapeutic strategies to enhance longevity and healthspan.

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