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Among captive chimpanzees, higher agreeableness males and higher openness females survive longer.

Increased production of ether lipids is required to extend lifespan in response to metformin, phenformin, and multiple, distinct, longevity-promoting manipulations, illuminating the possibility that raising ether lipid levels represents a new therapeutic strategy to support healthy aging.

Cell biological and genetic studies reveal age-associated alterations of lysosomes and modulation of lysosomal activity by longevity pathways.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

Profiling of fibroblasts across mammals captures differences in longevity at the level of global gene expression and metabolite levels and reveals pathways that define these differences.

The major cytosolic yeast peroxiredoxin Tsa1 controls aging and H₂O₂-resistance by inhibiting protein kinase A through a conserved cysteine in the catalytic subunit activation loop and not by scavenging H₂O₂.

Modulating the nutrient sensor TORC1 only in neurons in C. elegans is sufficient to regulate systemic longevity via inter-tissue signals that remodel mitochondria networks in non neuronal cells.

COVID-19 mRNA vaccine-elicited T cells recognize variants of concern and phenotypically differ depending on number of vaccine doses and prior SARS-CoV-2 infection status.

Clonotypic tracing of SARS-CoV-2–responsive T cells reveals vaccination-induced dominant Tfh clonotypes, not pre-existing T cells, associated with sustained humoral response, and can serve as an index of antigen-specific antibody longevity.

The dual control of adiposity and longevity emerges from a latent intestinal feedback loop which simultaneously augments fat loss and shields lifespan from the deleterious effects of continuous fat oxidation.