A study published today (January 12) in Cell provides evidence that epigenetic disruptions alone accelerate the molecular, physiological, and neurocognitive aging in mice, and that this is driven by the cellular response to DNA damage, such as double-strand breaks (DSBs). By activating specific genes highly expressed during mammalian development, the researchers were able to restore the epigenetic landscape disrupted by the DNA repair process in their aging mouse model, leading to signs of rejuvenation
Rapa will get you 10 of the years you need to wait. It is such an exciting time for the longevity field. I wish more people with money to invest in it were interested.
Before people get too hyped on “reprogramming” keep in mind that they havent done a single OSKM trail that considerably extends a healthy non-mutated mice beyond its normal maximum. Normal lab mice lives about 30 months or even 35
Signs of “rejuvenation” can be gamed, you can have a mice have younger skin have more energy but they dont live a single day longer or even die sooner.
Simple Fact: any real fix for aging will extend a mouses maximum lifespan way beyond its historic records. (nothing is stopping them from making a mouse live 6 , 7 , 8 years for demonstration)
" * A fate-tracing method for EpiSCs with DNA double-strand breaks (DSBs) was developed
EpiSCs with DSBs promptly differentiate to be selectively eliminated from the niche"
Any hypothesis as to the mechanism of aging has to explain all the known facts. One of the known facts is that there is something in blood that causes senescence to spread. Although I accept that aging is primarily an epigenetic issue (mitochondrial health is important as part of this) David Sinclair’s hypothesis does not explain this fact.
