In mice, deleting a long noncoding RNA drives premature aging.

A new device for isolating large quantities of old yeast cells expands the experimental boundaries of aging research.

Autophagic flux assays in the nematode Caenorhabditis elegans suggest that autophagy decreases during normal aging, whereas long-lived daf-2 and glp-1 mutants maintain autophagic capacity in distinct spatiotemporal-specific manners to extend lifespan.

Aging is a process characterized by gradual metabolome remodeling, deceleration of the remodeling in late life and under conditions that extend lifespan, and a mortality-associated pattern of cumulative damage.

The SAGA complex binds non-chromosomal DNA circles and prevents their spreading by attaching them to nuclear pores, thereby leading to the concomitant accumulation of DNA circles and pores in ageing yeast mother cells.

A protein called SIR-2.1 helps to protect worms from the effects of aging by regulating metabolic processes that would otherwise generate damaging reactive oxygen species.

A comprehensive mapping of the proteome and transcriptome during the complete replicative lifespan of budding yeast predicted an increased abundance of the protein biogenesis machinery is most causal for aging.

Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.

The aging lineage of budding yeast is differentiated by an early-appearing protein deposit that promotes protein quality control.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.