Sensationalizing no new mechanism

By: James V. Kohl | Published on: November 17, 2015

Scientists discover new mechanism that protects brain stem cells against aging-induced damage


Sebastian Jessberger says: This is an exciting new mechanism involved in stem cell division and aging. But as of now we are only just beginning to understand the molecular constituents and the true meaning of the barrier for stem cell division in the brain. One key question to be answered is whether the barrier is established in all somatic stem cells of the body.

My comment: There is no new mechanism of cell type differentiation. Protection against virus-induced genomic entropy in all cell types of all individuals is nutrient-dependent. Protection of all cell types is controlled by the physiology of reproduction in all living genera.

A barrier against brain stem cell aging

Before I was banned from commenting on news posts at, I wrote:

Excerpt: “One key question to be answered is whether the barrier is established in all somatic stem cells of the body. The answer to this question may open new routes to target age-dependent alterations of stem cell activity in human disease.”
My comment: Isn’t RNA-mediated cell type differentiation via the conserved molecular mechanisms of nutrient-dependent protein folding chemistry the most likely source of sex differences and somatic difference[s] in cell types in all living genera?
Claims about new mechanisms tell other pseudoscientists that they never learned enough about how cell type differentiation must occur. It occurs in the context of an atoms to ecosystems model of epigenetically-effected biophysically constrained RNA-mediated protein folding chemistry. Thermodynamic cycles of protein biosynthesis and degradation link metabolic networks and genetic networks to protein folding chemistry. RNA-mediated events link gene duplication and amino acid substitutions from supercoiled DNA to healthy longevity. Perturbed protein folding chemistry links viruses to all pathology.
Thanks to Emine Selcuk for alerting others to this via Longevity Turkey

See for comparison: New Enzyme Discovered for Sustaining Telomere Length
Excerpt 1)

…addition of de novo initiated telomeres (ADDIT) was used to observe an enzyme long suspected to be involved in telomere maintenance, ATM kinase. “ATM kinase was known to be involved in DNA repair, but there were conflicting reports about whether it had a role in telomere lengthening,” noted Dr. Greider.

Excerpt 2)

“Ultimately ADDIT can help us understand how cells strike a balance between aging and the uncontrolled cell growth of cancer, which is very intriguing.”

My comment: Claims that de novo initiated telomeres are intriguing can be used to limit investigation of nutrient-dependent de novo gene creation, which links the creation of new genes to enzyme-driven metabolic networks and back to genetic networks of DNA repair.
DNA repair can be viewed by all serious scientists in the context of models that link atoms to ecosystems in all living genera via supercoiled DNA and its protection against virus-driven genomic entropy.  There is no such thing as de novo supercoiled DNA or de novo cell type differentiation or de novo chromosomal rearrangements, which link ecological variation to ecological adaptations and all biomass.

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