Activation of the stress response pathway in young cells extends replicative lifespan, not by reducing global protein synthesis per se, but by Gcn4-mediated autophagy induction.

A high throughput, full lifespan microscopic analysis reveals that fission yeast does not age but has a finite replicative lifespan.

Reduced expression of a single transcription factor is sufficient to improve fitness and health at old age and increases the lifespan in female mice.

Genomic associations with lifespan principally reflect heart disease/smoking/dementia but not other cancers, and distinguish lifespan differences of five years between top/bottom deciles of a score derived from DNA alone.

Rare highly damaging mutations that are present in most human genomes decrease lifespan and are associated with an earlier onset of chronic diseases.

The dramatic extension of lifespan in Sirt6-deficient mice by Trp53 haploinsufficiency suggests that SIRT6 has distinct biological function from SIRT1 in regulating p53 activity and preventing cells from senescence/apoptosis.

The deacetylase Sir2 fine-tunes transcription of PMA1 and other aging related genes in a cAMP-PKA and CK2 signaling dependent manner.

A transcriptome-based metric for aging reveals a longevity mechanism that specifically prolongs the duration of young adulthood rather than slowing overall aging.

A robust mouse multi-tissue age predictor is presented that can be used to assess the DNA methylation age of mouse tissues and test the effects of longevity interventions.

Longevity in C. elegans is influenced not only by insulin/IGF-1 signalling, but also by CAMKII and calcineurin, acting on the same target, the transcription factor DAF-16.