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And do that in every living cell or how would that work? What about cells that don't replicate as much and just die off as you age?
by mburee 4y ago
And do that in every living cell or how would that work? What about cells that don't replicate as much and just die off as you age?
- derbOac 4y agoProbably CRISPR/Cas9 and other things (https://www.nature.com/articles/s41392-019-0089-y https://www.nature.com/articles/s41392-019-0089-y), but it seems like a useful thing to keep in mind as a target if somatic mutation accumulation is really behind aging, and we can now sequence whole genomes, and can also edit them. Even if you could target major aging pathways partially it would probably be of benefit. Large samples of whole genome sequencing has now been done, and as costs come down it should be possible to do extensive deep sequencing across some tissue samples and track people longitudinally, to see which somatic mutations, precisely, are associated with aging profiles. Then you could start by targeting gene editing of mutations in significant pathways. Gene therapy for congenital disorders in adults is now being done: https://www.science.org/content/article/first-gene-editing-treatment-injected-blood-reduces-toxic-protein-1-year https://www.science.org/content/article/first-gene-editing-t... https://www.axios.com/crispr-gene-editing-patient-ac724626-05cf-4584-b802-62e0e83388aa.html https://www.axios.com/crispr-gene-editing-patient-ac724626-0... https://www.aamc.org/news-insights/future-crispr-now https://www.aamc.org/news-insights/future-crispr-now If you think about aging as an acquired genetic disease, and gene therapy as an intervention, it makes sense.