Neonatal overfeeding accelerates age-related sarcopenia and metabolic disorders through lifelong gut mucosa and microbiota programming in mice

Hundreds of mitochondria in every cell work to produce adenosine triphosphate (ATP), a chemical energy store molecule needed to power cell activities.

A new study links an age-related decline in cellular maintenance to impaired immune clearance. Activating the pathway reduced signs of senescence in aged mice [1].

The immune system of the brain and body are distinct from one another, separated by the blood-brain barrier that lines blood vessels passing through the central nervous system.

Researchers here discuss the chronic inflammation of aging as a contribution to the bidirectional relationship between the loss of bone mineral density leading to osteoporosis and neurodegenerative pathology leading to cognitive impairment.

Investigating age-related remodeling of lipid species to shed light on the molecular underpinnings of aging, here Li et al. show that lipid acyl chains become longer with age. Lipid elongation occurs across species, tissues and during heart disease progression.

Genetic influences on complex traits change over the lifespan. Schoeler et al. show that cross-sectional and longitudinal studies can give different estimates of how genetic effects change with age, mainly owing to birth cohort differences and participation bias.

Li and colleagues identify lipid acyl chain elongation as a conserved hallmark of aging across tissues and species. Genetic shortening of lipid chains extends lifespan in worms, which establishes chain length as a causal contributor to aging.

Longitudinal multiomics reveals personalized aging trajectories

Author Correction: Age-, sex- and proximal–distal-resolved multi-omics identifies regulators of intestinal aging in non-human primates

Popular weight-loss drugs may do more than help people shed pounds. They might also melt away the years. Drug giants Eli Lilly and Novo Nordisk say patients taking their drugs age less quickly, according to readouts from molecular “aging clocks.”