It's no longer remarkable for researchers to discover ways to alter genes or the level of proteins produced through gene expression that extend life in laboratory animals. Many new interventions of this sort are discovered every year, and most go largely unremarked now. With the falling cost and increasing capacity of DNA sequencing and related biotechnologies it is becoming ever easier to find new connections or poke and prod at DNA and protein machinery in living organisms. That trend speeds the pace of progress in this field, and here is a recent example:
Mit mutations that disrupt function of the mitochondrial electron transport chain can, inexplicably, prolong Caenorhabditis elegans lifespan. In this study we use a metabolomics approach to identify an ensemble of mitochondrial-derived α-ketoacids and α-hydroxyacids that are produced by long-lived Mit mutants but not by other long-lived mutants or by short-lived mitochondrial mutants.
We show that accumulation of these compounds is dependent upon concerted inhibition of three α-ketoacid dehydrogenases that share dihydrolipoamide dehydrogenase (DLD) as a common subunit, a protein previously linked in humans with increased risk of Alzheimer's disease. When the expression of DLD in wild type animals was reduced using RNA interference we observed [that] as RNAi dosage was increased lifespan was significantly shortened but, at higher doses, it was significantly lengthened, suggesting DLD plays a unique role in modulating length of life.