Nature Medicine | Spoonful of Medicine

Understanding aging

Three papers published this past Sunday touch upon different aspects of the aging problem. The first one appeared in Nature and is authored by Rui Yi and colleagues, who found that microRNA-203 promotes the differentiation of skin stem cells by repressing “stemness”. In stratified epithelia, stem cells located basally are crucial for self renewal. As these cells leave the basal zone, they differentiate and cease to behave like stem cells. What the authors found is that microRNA-203 is crucial for this differentiation process, leading the stem cells to exit the cell cycle. Mechanistically, this effect depends on repression of p63 expression, a molecule that had previously been shown to regulate stem-cell maintenance in epithelia.

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The second one is on one of my favorite topics — progeria. Writing in Nature Cell Biology, Paola Scaffidi and Tom Misteli report that expression of mutant lamin-A, the molecule that causes Hutchinson-Gilford Progeria Syndrome (HGPS), interferes with the function of human mesenchymal stem cells (hMSCs) by promoting the activation of downstream

effectors of Notch, affecting the differentiation potential of hMSCs. The in vivo relevance of these results to HGPS and to normal aging remains to be established, but the possibility is indeed tantalizing.

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The third one is a Brief Communication in Nature Genetics. In it, Marc Vermulst and his colleagues establish a link between mitochondrial DNA (mtDNA) deletions and aging in the so-called Polga mice, which harbor a proofreading-deficient copy of polymerase gamma and are characterized by premature aging. They found that the rate at which different tissues accumulate mtDNA mutations before they reach phenotypic expression differs profoundly — brain, heart and gut are among the most affected parts of the body. The question remains, though, if these mtDNA mutations are also relevant during normal aging in wild-type mice and, of course, in humans.

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    Sergio Stagnaro MD said:

    As a researcher in the field of Quantum Biophysical Semeiotic since 52 years, I am concerned at human health, rather than that of mice. However, it is really interesting that also these Authors have been observing mitochondrial alterations in skin of aging mice , as I have been suggesting since 1982, when I discovered a singular functional mitochondrial cytopathy, conditio sine qua non of all common and severe human diseases, i.e., Congenital Acidosic-Enzyme Metabolic Histangiopathy (Ash Google.com). Whatever mit-DNA and n-DNA gene mutation unavoidably causes alteration of biological system activity. In our cases, i.e., skin aging, due to mitochondrial impairment, there is always biophysical-semeiotic Co-Q10 deficincy syndrome. Therefore, from the clinical viewpoint, it proved to be very helpful in recognizing individuals to undergo sophisticated and expensive laboratory research, regarding such as

    interesting disorder, diagnosed since early stage. In fact, I demonstrated earlier that doctors can clinically recognize subjects involved by Ubidecarenone deficiency, even

    initial and symptomless (ibidem; and in my website, known to NATURE). In addition, in my long clinical experience, such as diagnosis, made bedside with a stethoscope for the first time, proved to be

    really efficaious and reliable in avoiding dangerous administration of

    such as drug to individuals without clinical sintomatology and only apparently healthy, but involved by

    ubidecarenone deficiency, notoriously worsened by anti-cholesterolemic

    drugs. In conclusion, skin early aging may indicate an underlying serious Co-Q10 deficiency.