Clonal Mutation in Immune Cells Correlates with Epigenetic Age Acceleration

The nuclear DNA encoding near all of the protein machinery necessary to cell function is constantly damaged and constantly repaired. The repair mechanisms are highly efficient, and are backed up by numerous other systems intended to destroy cells that suffer particularly critical DNA damage, mutations that can lead to cancer or severe dysfunction. Nonetheless, damage accumulates. Near all of this damage is irrelevant, as it occurs randomly in single somatic cells with a limited life span, in genes that the cell isn't using. Unfortunately, there are ways for DNA damage to become significant. The first is obviously cancer, a condition arising from particular combinations of mutational damage that allow a cell to replicate aggressively without limit. The second is when damage occurs in a stem cell or progenitor cell that will create large numbers of descendant somatic cells. A mutation can be spread widely throughout a tissue, and the resulting patchwork of mutations is known as somatic mosaicism. It is thought that somatic mosaicism contributes to the general level of dysfunction in aging tissue, but this is hard to prove at the present time: the compelling experiment that isolates only this class of nuclear DNA damage as a factor and links it to specific aspects of aging has yet to be designed and carried out. It is easy to generate nuclear DNA damage in animal models, via radiation or genetic engineering to disable repair mechanisms, and indeed this causes harm, but it...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs