Single-cell transcriptomics reveals altered pathways, gene expression dynamics, and activation of transcriptional programs in human early hematopoiesis during healthy aging and myelodysplastic syndromes.

Older people can recruit additional brain regions to help perform complex tasks, possibly compensating for age-related changes in other parts of the brain.

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.

Deep and comprehensive proteomic resource of human intervertebral disc at high spatial resolution with a methodological flow reveals new insights in disc homeostasis and degeneration.

Identification of human DNA sites differentially methylated with aging across six different primary immune cells suggests that the sensing of hypoxia drives the epigenetic clock.

Identification of causal genes and their effects on other biological determinants untangles the complexities of aging and Alzheimer's and can facilitate drug discovery for sustaining healthy aging and treating Alzheimer's.

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

Older PhenoAge was consistently related to an increased risk of incident cancer with adjustment for chronological age and the aging process could be retarded by adherence to a healthy lifestyle.

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.