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.

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.

MicroRNA-146b regulates aging, activation, and mitochodrial function in thioglycollate-elicited peritoneal macrophages.

Modulation of histone levels in gut enterocytes by rapamycin treatment alters chromatin organisation and induces intestinal autophagy through transcriptional regulation to prevent age-related decline in the intestine and extend lifespan.

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

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.

Transcriptional analyses provide an atlas of how traumatic brain injury and aging shape meningeal cell composition and gene expression.

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