DunedinPACE is a novel DNA methylation biomarker of the pace of biological aging for intervention trials and natural experiment studies investigating how the rate of aging may be changed by behavioral or drug therapy, or by environmental modification.

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.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

Breast luminal epithelial cells are the hotspots of aging-associated changes, which prime aged epithelia for oncogenic gene activation and may explain individual differences in breast cancer susceptibility due to the aging-associated increase in gene expression variances in luminal epithelia.

While tau and aging have highly overlapping differential gene expression signatures, they diverge in the affected cell types, with aging having a wide-ranging impact and tau-triggered changes instead polarized to excitatory neurons and glia.

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.

Cross-sectional transcriptome analysis of mice, covering the whole lifespan, reveals that inter-tissue divergence during development is accompanied by a weaker but widespread convergence during ageing.

Activation of a DNA-damage cell cycle checkpoint during aging causes genome instability and senescence in yeast mother cells.

Tom70 connects the mitochondrial import to the nuclear transcriptional activity of mitochondrial proteins and controls mitochondrial biogenesis defects during aging.

The accumulation of somatic mutations during aging is not uniform across tissue types and, in addition, shows significant variability in the source of mutation that can be modified by small molecule interventions.