Detectable clonal mosaicism frequency in peripheral blood is low (<0.5 %) from birth until 50 years of age, after which it rapidley rises to 2-3% in the elderly [22561516].The frequency of mosic abnormalities increases with age, from 0.23% under 50 years to 1.91% between 75 and 79 years [22561519]. DNA damage drives aging, in part by activating NF-kabbaB. Inhibition of NF-KabbaB reduces oxidative stress, DNA damage, protein damage, and cellular senescence induced by oxidative damage [Preventing Cellular Aging And Aging-Related Degenerative Diseases].

Acquired differences in structural chromosome variants between members of monozygoutic twin pairs (including mosaic anomalis) are observed in pair

DNA damage, mutations and genome instability accumulate with age [23,24,38].

DNA repair capacity decreases with age [23,42].

Why do giant animals such whales do not get cancer, besides the enormous demand on cell division to build such huge bodies? How can DNA damage be the major driver of aging if each generation inherits the DNA from us, but has a total restored lifespan? Is the germ line so much more protected compared to the somatic cells? Is the are very good selection mechanisms which eliminates all DNA damaged cells (how can it be)? Are the types of DNA damages which accumulate with age are all repaired before passing to the next generation? Does ectopic/forced damage to the germ cells genome results in premature aging progeny?

Tags: aging