The gene is called Parkin, and when defective is implicated in the development of Parkinson’s disease.
The gene normally functions to recycle cell proteins and defective mitochondria. It acts to tag defective structures so they are degraded an recycled. It tags them by adding a ubuquitin to the protein’s surface.
It seems clear that at least in part, aging is due both to accumulation of damaged and misfolded proteins in the cell, and increasing numbers of defective and leaky mitochondria, the latter of which release reactive oxygen species which then lead to further damage.
So it seems plausible that if it were possible to amplify the functioning of the cellular garbage disposal system, aging might be reduced.
Amazingly this is just what was found.
When parkin was genetically overexpressed in all cells of fruitfiles they exhibited a dramatic 28% increase both in mean and more importantly maximum lifespan. In addition these long lived flies showed no loss of function and appeared healthy.
The authors conclude:
Our work strongly suggests that treatments designed to augment Parkin expression during aging may delay the onset and progression of a number of age-onset diseases
Of course we cannot genetically modify adult humans, however the development of small molecules which can either activate, enhance or mimic Parkin within cells could lead to dramatic increases in healthy human lifespan.