Might interest some, mentions telomeres.

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Aging is a common factor in many diseases. So, what if it were possible to treat them by acting on the causes of aging or, more specifically, by acting on the shortening of telomeres, the structures that protect chromosomes? This strategy is being pursued by the Telomeres and Telomerase Group of the Spanish National Cancer Research Centre (CNIO), which has already succeeded in curing pulmonary fibrosis and infarctions in mice by lengthening telomeres. Now they take a first step towards doing the same with renal fibrosis by demonstrating that short telomeres are at the origin of this disease, which is also associated with aging.

The new study will be published this week in the journal Nature Aging.

Renal fibrosis is the most common cause of kidney failure, a disease that can currently only be treated by dialysis. It is characterized by excessive scarring of the tissue, which hardens and loses its functionality.

But such drugs could face a daunting challenge, since aging is not considered a disease. This means the Food and Drug Administration is unlikely to approve a drug for its anti-aging effects, or as a new use for a licensed drug. Also, pharmaceutical companies probably wouldn’t be inclined to develop drugs for that purpose only.

Drugs that can postpone or prevent the onset of debilitating diseases could enhance longevity and provide enormous societal benefits, geroscientists say.

Real aging reversal!

The hematopoietic (blood-forming) stem cells (HSCs) residing in our bone marrow produce all of our blood cells, including key immune cells that protect us from bacteria and viruses. As we age, our HSCs become less efficient and less able to make healthy new blood cells. In a study published online today in Nature, researchers at Albert Einstein College of Medicine have found that this reduction in HSC efficiency is caused in part by the deterioration of chaperone-mediated autophagy (CMA), the housekeeping process that removes damaged proteins and other waste materials that interfere with cells’ ability to function.

“While the aging of HSCs in our bone marrow is inevitable, the good news is that it may be reversible,” said co-study leader Ana Maria Cuervo, M.D., Ph.D., professor of developmental and molecular biology, of anatomy and structural biology, and of medicine, and the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases at Einstein. “Our studies in mice suggest that drugs we’ve developed at Einstein can activate CMA and potentially restore the vitality of HSCs in older people.”