This is, at least, for worms based on investigations into the cellular recycling protein, which shows how expression of this protein is key. Researchers based at Sanford Burnham Prebys Medical Discovery Institute, have demonstrated how worms live longer lives provided they produce excess levels of p62. This protein can recognize toxic cell proteins that are tagged for destruction.
The significance of the experimental findings are that they could open the door to treatments for age-related conditions, including neurodegenerative conditions like Alzheimer’s disease (where the prevailing theory is that the disease is caused by the accumulation of misfolded proteins).
According to lead researcher Professor Malene Hansen: “Research, including our own, has shown that lifespan can be extended by enhancing autophagy — the process cells use to degrade and recycle old, broken and damaged cell components.” Autophagy, as part of normal biological function, allows the orderly degradation and recycling of cellular components.
For the research studies, the short-lived, transparent roundworm Caenorhabditis elegans was used as the model organism. It is a suitable organism because the nematode’s cell lineage has been mapped and its genome fully sequenced, allowing scientists to note even the smaller genetic variations.
To assess the role of p62, the research team genetically engineered C. elegans to produce excess levels of the protein p62. Instead of their usual three-week lifespan, these worms lived for a month (or what would be a 20 to 30 percent lifespan extension).
The next phase of the research will involved assessing what types of harmful cellular ‘trash’ p62 is removing, and then seeing what difference this plays in address age-related diseases like Alzheimer’s.
The research has been published in the journal Nature Communications. The research paper is titled “The autophagy receptor p62/SQST-1 promotes proteostasis and longevity in C. elegans by inducing autophagy.”
