As they age, mammalian cells accrue distinct epigenetic signatures—for example, variations in DNA methylation patterns. Yet it has remained unclear whether these are a cause or a consequence of aging. A study published today (January 12) in Cell provides evidence that epigenetic disruptions alone accelerate the molecular, physiological, and neurocognitive aging in mice, and that this is driven by the cellular response to DNA damage, such as double-strand breaks (DSBs). By activating specific genes highly expressed during mammalian development, the researchers were able to restore the epigenetic landscape disrupted by the DNA repair process in their aging mouse model, leading to signs of rejuvenation.
DSBs have long been associated with aging. Because this severe form of DNA damage can lead to mutations, some researchers have hypothesized that this derived accumulation of genomic alterations could be a major cause of aging. However, in recent decades, other data have hinted that DNA ...
