Older genomes have more dodgy genes

Nutrient-sensing systems can be tuned up; senescent cells targeted for destruction; stem cells supplied afresh; epigenomes spruced up. For many of the hallmarks of ageing hope is in the air. But some are more refractory. Perhaps the toughest of all is genomic instability: the persistent accumulation of mutations. By middle age, to take an example published in 2018 by Philip Jones’s group at the Wellcome Sanger Institute near Cambridge, England, the cells lining a human oesophagus will each have acquired mutations in an average of 20 genes.