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The rapid development of immune memory in infancy shapes the composition of T cell defenses throughout the human lifespan.

There is now sufficient and diverse evidence to support a cogent argument that DNA damage plays a causal role in aging.

Declining TFEB and autophagy levels with age are key to poor vaccination efficacy in the elderly.

Biological aging processes and age-related diseases demonstrate sexual dimorphism where complex interactions between underlying aging mechanisms and sex chromosomes and hormones are seen in humans and animals.

Circulating cell-free DNA studies should control for participants' physical activity to avoid its confounding effect on total cell-free DNA level.

Despite no observed correlation between retrotransposon (RTE) activity and chronological age, the expression of most RTE classes and families except SINEs correlated with biological age-associated gene signature scores.

Lithocholic acid associates with skeletal muscle mass and plays an important role in skeletal muscle hypertrophy through activation of the bile acid receptor.

Translational evidence indicates APOE2 benefits longevity independent of its protective effects on Alzheimer’s disease, which preserved activity and the metabolism of apoE protein and associated-lipids would be key to understanding.

Light controls can fine tune microbiome–host interaction to qualitatively regulate host longevity with temporal and spatial precision.

Adiponectin is an essential regulator for healthspan and is indispensable for sustaining a normal lifespan.