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Scientists have traditionally studied diseases separately because they have separate pathologies. Heart disease mostly comes from accumulated fat deposits clogging arteries, cancers from DNA damage, Alzheimer’s and other dementias from damaged brain cells, etc.—and each disease has multiple contributing factors. But they share a common feature: Aging drives them all. If we delay aging and rejuvenate organs, tissues, and cells, we can prevent or remediate them all. According to Nir Barzilai, director of the Institute of Aging Research at Albert Einstein College of Medicine, “Although aging is the major risk factor for developing most adult-onset diseases, systematic investigations into the fundamental physiology, biology, and genetics of aging are only just beginning.”
There’s good reason to be confident that moving away from the “infectious disease” model and shifting research dollars from individual diseases of aging to the basic biology of aging will be productive. Not only because such a shift upgrades the theoretical model on which research is based, but because it already has been. A seminal paper in this field was published in Nature in 2005. “Rejuvenation of aged progenitor cells by exposure to a young systemic environment” had profound implications and initiated multiple lines of investigation being actively pursued by the scientists involved in the original experiments and by many others in labs at universities, research institutions, and pharmaceutical companies around the world.
https://www.tabletmag.com/jewish-news-and-politics/201752/beyond-120
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