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Encouraging news in rejuvenation research


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Yeah, I saw that story floating around today, but I can't make heads or tails of it. Does the 30% life extension apply only to the accellerated aging mice? If yes, then I guess good for the premature aging mice - but all it does is correct the underlying pathology. If it did it in normal lifespan mice and extended that by another 30% that would be something to write home about. Also, if it rejuvenates the cells by bringing them to an earlier stage of development, why couldn't you keep doing that over, and over again - so if you can reverse aging, then every time you hit a certain age you could just reverse again... right? If not, and you can only do that once, I guess that's still useful (in a normal lifespan organism). 


In short, it's hard to tell just what these guys have accomplished. Plus, there is always the issue of neural tissue in the brain - at some point you are at risk of losing your identity if there is too much replacement of tissue that forms your memories and the like. 


Bottom line: interesting, but way too little info on display here.

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In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming

Online Extra

Alejandro Ocampo, Pradeep Reddy, Paloma Martinez-Redondo, Aida Platero-Luengo, Fumiyuki Hatanaka, Tomoaki Hishida, Mo Li, David Lam, and others

Cell, Vol. 167, Issue 7, p1719–1733.e12

Published in issue: December 15, 2016


•Partial reprogramming erases cellular markers of aging in mouse and human cells

•Induction of OSKM in progeria mice ameliorates signs of aging and extends lifespan

•In vivo reprogramming improves regeneration in 12-month-old wild-type mice


Aging is the major risk factor for many human diseases. In vitro studies have demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of the aging process through reprogramming has not been directly demonstrated in vivo. Here, we report that partial reprogramming by short-term cyclic expression of Oct4, Sox2, Klf4, and c-Myc (OSKM) ameliorates cellular and physiological hallmarks of aging and prolongs lifespan in a mouse model of premature aging. Similarly, expression of OSKM in vivo improves recovery from metabolic disease and muscle injury in older wild-type mice. The amelioration of age-associated phenotypes by epigenetic remodeling during cellular reprogramming highlights the role of epigenetic dysregulation as a driver of mammalian aging. Establishing in vivo platforms to modulate age-associated epigenetic marks may provide further insights into the biology of aging.

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