A Study of DNA Alterations in the Old
To what degree does nuclear DNA damage contribute to aging? That remains a debated question. Here, researchers show that, at least in immune cells, there are perhaps more forms of large DNA damage than thought in the old: "researchers compared the DNA of identical (monozygotic) twins of different age. They could show that structural modifications of the DNA, where large or small DNA segments change direction, are duplicated or completely lost are more common in older people. The results may in part explain why the immune system is impaired with age. During a person's life, continuous alterations in the cells' DNA occur. The alterations can be changes to the individual building blocks of the DNA but more common are rearrangements where large DNA segments change place or direction, or are duplicated or completely lost. ... The results showed that large rearrangements were only present in the group older than 60 years. The most common rearrangement was that a DNA region, for instance a part of a chromosome, had been lost in some of the blood cells. ... Rearrangements were also found in the younger age group. The changes were smaller and less complex but the researchers could also in this case show that the number of rearrangements correlated with age. ... We were surprised to find that as many as 3.5 percent of healthy individuals older than 60 years carry such large genetic alterations. We believe that what we see today is only the tip of the iceberg and that this type of acquired genetic variation might be much more common. ... The researchers believe that the increased number of cells with DNA alterations among elderly can have a role in the senescence of the immune system. If the genetic alterations lead to an increased growth of the cells that have acquired them, these cells will increase in number in relation to other white blood cells. The consequence might be a reduced diversity among the white blood cells and thereby an impaired immune system." Compare that with the other explanations for reduced diversity that involve persistent and pervasive viruses like CMV.
Link: http://www.eurekalert.org/pub_releases/2012-02/uu-itr012612.php
So, is the only way to repopulate our cells with the correct DNA to replace each cell population in its entirety? If every cell has its own epigenetic characteristics, it wouldn't be possible to swap chromosomes of every cell with a single universal copy, right?
@Patrick: You're right in thinking that global DNA repair of stochastic cell-specific damage is hard. You might look at the chromallocyte proposal for the sort of technology needed:
https://www.fightaging.org/archives/2007/04/an-interview-with-robert-freitas.php
So we should hope that nuclear DNA damage isn't as anywhere near as important as other contributions to aging - which may be the case:
https://www.fightaging.org/archives/2010/11/is-nuclear-dna-damage-a-cause-of-aging.php
@Reason - Nuclear DNA alterations may be important only for certain rapidly dividing cell populations. In that case, renewal of the stem cell pools through cell therapy from carefully chosen genetically intact cells could suffice. Alternatively, it could be that a stressful inter-cellular environment such as is brought about by other kinds of aging leads to cells being more sloppy in the maintenance of their genomic integrity. In that case, fixing the other causes of aging would have a large collateral benefit.