Cells of the same age follow dramatically different biological aging paths

Researchers at Hebrew University, in collaboration with Altos Labs and the Babraham Institute, performed single-cell analysis of DNA methylation across multiple mouse and human tissues. The study found that cells with identical chronological age can follow dramatically different biological aging trajectories. Most cells remained relatively young, while a smaller subset aged much faster, accumulating molecular changes associated with aging. Tissues became mosaics of young and old cells. Rapidly dividing cells were more likely to enter the fast-aging state. In one experiment, white hairs from the same individual consistently carried older epigenetic signatures than black hairs, providing visible evidence that aging occurs at the individual cell level. Cells with advanced epigenetic aging showed altered gene activity in pathways linked to immune function, protein production, neurodegeneration, and tumor development. The pattern was not universal: some tissues aged more uniformly than others. The findings may explain why age-related diseases like cancer and neurodegeneration often originate in a small number of cells before expanding.

Aging is not a uniform process across cells, and individual cells may transition into an accelerated aging state before age-related disease becomes detectable at the tissue level.