Researchers have discovered that lifespan can be extended by enhancing the process cells use to degrade and recycle old, broken and damaged cell components.
Scientists have shown that worms live longer lives if they produce excess levels of a protein, p62, which recognises toxic cell proteins that are tagged for destruction.
The discovery could help uncover treatments for age-related conditions, such as Alzheimer’s disease, which are often caused by accumulation of misfolded proteins.
Scientists used to think that cellular recycling worked the same way for all waste products.
In more recent years, researchers are learning that autophagy (the process cells use to degrade and recycle old, broken and damaged cell components) can be highly selective – meaning the cell uses distinct ‘recycling trucks’, such as the protein p62, to deliver different types of trash to cellular ‘recycling centres’. For example, p62 is known to selectively deliver aggregated proteins and worn-out mitochondria (the powerplants of the cell) to recycling centres.
To better understand p62’s role in cellular recycling and longevity, the scientists used short-lived, transparent roundworms called C. elegans for their studies.
Previously, the research team found that levels of p62 were increased after a short heat shock was administered to the worms. This proved to be beneficial to the animals and required for the longevity caused by mild heat stress.
These findings prompted the scientists to genetically engineer C. elegans to produce excess levels of the protein p62.
Instead of their usual three-week lifespan, these worms lived for a month – equivalent to a 20 to 30 per cent lifespan extension.
The researchers were intrigued to find that by increasing the levels of p62 (the ‘recycling truck’), the ‘recycling centres’ became more abundant and were able to recycle more ‘trash’, indicating that p62 is a driver of the recycling process.
“Now that we have confirmed that selective autophagy is important for longevity, we can move to our next step: identifying what harmful cellular ‘trash’ it is removing,” explained lead author Dr Caroline Kumsta.
“With this knowledge, we hope to target specific cell components that are risk factors for longevity.”
Many age-related diseases, including Alzheimer’s and Huntington’s disease, are caused by accumulation of toxic, misfolded proteins.
Scientists are hopeful that studying selective autophagy via proteins like p62 could lead to therapies that clear the proteins that are detrimental to living a long, healthy life.
Translating this research to humans could however be problematic as high levels of p62 have been shown to be associated with cancer.
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