Short-term treatment with rapamycin reverses periodontal bone loss, attenuates inflammation, and remodels the oral microbiome toward a more youthful state.

The changes in the skeletal muscle proteome with age indicate the roots of the decline in muscle function with age.

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

Methylation pace of aging is a novel measure requiring only a blood sample that clinical-trial and observational studies can use to test if treatments modify how fast participants are aging.

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.

Biological ages have the potential to provide aging-related information beyond chronological age and can be predictive of mortality independently of both chronological age and different types of biological ages.

A minor subset of plasma lipids are heritable, and this is associated with gene expression of transcripts related to roles beyond lipid metabolism, including immune function and cell signalling.

In the fruit fly Drosophila melanogaster, stem cell activity ages female guts but not male guts; furthermore, males with feminized guts develop pathologies but gain an increase in lifespan through dietary restriction.

Metabolic health and longevity can be separated by ovariectomy, which also protects female mice lacking hepatic mTORC2 from midlife mortality.

The concept of compound fracture risk is redefined to combine the risk that an individual will sustain a fracture and the risk of mortality once the fracture has occurred.