@adssx kindly referred a paper to me that seems to explain the reasons why some old experiments with DNA had quite significant lifespan benefits for rodents.
1.4_Part_1.445.pdf (731.0 KB)
j.1532-5415.1973.tb01207.x.pdf (202.6 KB)
Robertson 1928 nucleic acids upon the growth and longevity of the white mouse.pdf (5.1 MB)
Thanks for writing this.
The paper (U Gothenburg + Max Plank Institute): Ribonucleotide incorporation into mitochondrial DNA drives inflammation 2025
To test whether the increased rNMP content of mtDNA affects mtDNA release and SASP, we treated senescent cells with deoxyribonucleosides. Deoxyribonucleoside supplementation did not affect the senescent state per se as assessed by monitoring SA-β-gal activity (Extended Data Fig. 9h). However, it significantly reduced cytosolic mtDNA (Fig. 5c and Extended Data Fig. 9i) and the mtDNA sensitivity for alkali and RNase H2 treatment, indicating a lower rNMP content (Fig. 5c,d).
News report: Mitochondria Dump Their Rubbish DNA, And It Could Be Costing Us Our Health 2025
I do reference the paper in my blog post. I think the sciencealert summary is wrong. They say:
That rejection is potentially one of the key drivers behind the inflammation that comes with old age, and the negative health consequences associated with it – from certain types of cancer to neurodegenerative diseases like Alzheimer’s.
“This response provides protection against pathogens but can also promote autoimmune and inflammatory diseases and contribute to senescence and aging,” write the researchers in their published paper.
It’s yet to be determined how much this type of inflammation occurs during the normal aging process, or whether it takes place under specific conditions.
Humans are living longer than ever before, and that means all of the biological machinery in our bodies is working overtime. As the years go by, stress, damage, and inflammation stack up, leading to poor health.
If we can understand more about how to cut out some of that damage – how to stop mtDNA making these particular mistakes in replication, for example – then we’re possibly on the way to developing ways of keeping our cells in better shape in old age.
This implies they see the rejection of the flawed DNA as being the issue rather than the creation of the flawed DNA.
IMO it is very obvious that this is a mechanism that enables improved replication of mtDNA. Exactly how to do this is not yet that clear. However, I will spend some time reading up on this as it is a new dimension of interventions.