Applying big-data analytic techniques to brain images from 18,707 individuals is shedding light on the influence of aging on the brain.

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.

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 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.

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.

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.

Two novel subsets of microglia identified by their unique autofluorescence profiles differ in their subcellular organization, proteomic signatures and in their response to aging and lysosomal dysfunction.

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