A Method of Inducing Epigenetic Aging via Damage to DNA

You may recall the work linking DNA double strand break repair to epigenetic changes characteristic of aging. Repeated cycles of this repair cause some form of depletion of necessary factors or other disarray in the mechanisms controlling gene expression. This is a compelling way to link random DNA damage, largely occurring in parts of the genome that are inactive in any given cell, largely occurring in cells that will not go on to divide many times, and occurring in completely different locations from cell to cell, to a consistent, characteristic aspect of aging. Beyond the question of cancer risk, the only other compelling way to connect stochastic DNA damage to the general declines of aging is to consider somatic mosaicism emerging as a result of mutational damage to stem cells, as that mutation spreads throughout a tissue. In today's materials, researchers describe a way to accelerate this epigenetic change caused by repair of breaks in DNA, and characterize a mouse lineage engineered to undergo a great deal of DNA damage, but damage that occurs only in inactive portions of the genome, and should thus produce no harm to the genomic information needed for cell function. The result appears to be accelerated aging, occurring though the mechanism of epigenetic change noted above. This allows researchers to more readily test the use of partial reprogramming as a means to reverse this epigenetic change, and better understand how this reversal works. As ever, one s...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs