Autophagy is the name given to the collection of cellular processes that recycle broken and unwanted proteins and cell structures. More autophagy is a good thing, and many of the methods demonstrated in the laboratory to modestly slow aging in flies, worms, and mice involve enhanced autophagy. You might look at a recent experiment demonstrating a 10% gain in mouse life span via a narrowly targeted method of increasing autophagy, for example. Calorie restriction, the gold standard in reliability when it comes to slowing aging, depends upon autophagy: it doesn’t work when autophagy is disabled.
Unfortunately, autophagy declines with age. But why? There are undoubtedly many answers to that question, a layered set of mechanisms that directly or indirectly arise from the root causes of aging, the accumulation of molecular damage as outlined in the SENS rejuvenation research proposals. In the direct case, autophagy suffers because persistent metabolic waste accumulates in lysosomes, the structures responsible for disassembling proteins and cell components. They are packed full of enzymes capable of dismantling near all of what they encounter, but near all isn’t good enough over the long term. Long-lived cells in older people
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