An Israeli study came out last week that has been described as rejuvenation via hyperbaric oxygen. I’m not taking it very seriously, and I owe you an explanation why.
According to new research from CCR scientists, embryonic stem cells have a unique way of protecting their telomeres, the structures at the ends of chromosomes that shorten with every cell division. A research team led by Eros Lazzerini Denchi, Ph.D., an NIH Stadtman investigator in CCR’s Laboratory of Genomic Integrity, has found that rather than treating exposed telomeres as damaged DNA as most cells do, embryonic stem cells call on genes typically used only during the earliest stage of development to stave off unwanted DNA repair. The team’s findings, which come from studies of mouse embryonic stem cells, are reported November 25, 2020, in Nature.
By revealing an unexpected way cells can protect their telomeres, the new findings may help explain a survival strategy employed by some cancer cells, which must find a way to circumvent growth limits imposed by the natural shortening of telomeres that occurs as we age.
Embryonic stem cells, which arise early in an embryo’s development, have a unique capacity to become virtually any of the body’s specialized cell types. Lazzerini Denchi and colleagues first discovered their unusual approach to protecting telomeres when they found that the cells can survive without a protein called TRF2, which binds to and protects chromosome tips. The protein is absolutely essential for hundreds of different types of cells. Without it, exposed chromosome tips trigger faulty activation of DNA damage repair pathways, which stitch the unprotected ends together. Chromosomes fuse together and cells lose the ability to divide. But when Lazzerini Denchi’s team removed TRF2 from embryonic stem cells, chromosomes maintained their integrity and the cells continued to proliferate.
These findings […] strongly suggest that high levels of iron in the blood reduces our healthy years of life, and keeping these levels in check could prevent age-related damage.
Genes linked to ageing that could help explain why some people age at different rates to others have been identified by scientists.
The international study using genetic data from more than a million people suggests that maintaining healthy levels of iron in the blood could be a key to ageing better and living longer.
The findings could accelerate the development of drugs to reduce age-related diseases, extend healthy years of life and increase the chances of living to old age free of disease, the researchers say.
Might interest some as it mentions telomeres.
The historic NASA Twins Study investigated identical twin astronauts Scott and Mark Kelly and provided new information on the health effects of spending time in space.
Colorado State University Professor Susan Bailey was one of more than 80 scientists across 12 universities who conducted research on the textbook experiment; Mark remained on Earth while Scott orbited high above for nearly one year. The massive effort was coordinated by NASA’s Human Research Program.
Bailey has continued her NASA research and now joins more than 200 investigators from dozens of academic, government, aerospace and industry groups to publish a package of 30 scientific papers in five Cell Press journals on Nov. 25.
Here’s my latest video!
Meta-analysis for the association between HDL with all-cause mortality risk has identified HDL levels 55 — 60 mg/dL range as optimal. However, that data includes subjects up to 85y-in the video, I present data for 85y — 115yr olds that additionally suggests HDL in the 55 — 60 mg/dL range as optimal. In addition, I show my own HDL data over the past 15 years (n=34), the correlation for HDL with my diet, and how I plan on consistently increasing my 15-year average HDL of ~44 mg/dL to the 50’s.
10% longer.
Reduced food intake, known as dietary restriction, leads to a longer lifespan in many animals and can improve health in humans. However, the molecular mechanisms underlying the positive effects of dietary restriction are still unclear. Researchers from the Max Planck Institute for Biology of Aging have now found one possible explanation in fruit flies: they identified a protein named Sestrin that mediates the beneficial effects of dietary restriction. By increasing the amount of Sestrin in flies, researchers were able to extend their lifespan and at the same time these flies were protected against the lifespan-shortening effects of a protein-rich diet. The researchers could further show that Sestrin plays a key role in stem cells in the fly gut thereby improving the health of the fly.
The health benefits of dietary restriction have long been known. Recently, it has become clear that restriction of certain food components, especially proteins and their individual building blocks, the amino acids, is more important for the organism’s response to dietary restriction than general calorie reduction. On the molecular level, one particular well-known signaling pathway, named TOR pathway, is important for longevity.
“We wanted to know which factor is responsible for measuring nutrients in the cell, especially amino acids, and how this factor affects the TOR pathway,” explains Jiongming Lu, researcher in the department of Linda Partridge at the Max Planck Institute for Biology of Aging. “We focused on a protein called Sestrin, which was suggested to sense amino acids. However, no one has ever demonstrated amino acid sensing function of Sestrin in a living being.” Therefore, Lu and his colleagues focused on the role of Sestrin in the model organism Drosophila melanogaster, commonly known as fruit fly.
Important that people read this given how much this spread.
If you have been following the mainstream media recently, you have probably seen a story about hyperbaric oxygen treatment and claims that it can reverse aging. Unfortunately, the media hype surrounding the results is nothing like the reality of the actual research paper, and this is another example of how shoddy journalism harms our field.
Welcome to the media circus
Back in July, we talked about how hyperbaric oxygen therapy may reduce age-related cognitive decline in older people, which was based on the results of another study. A new publication from the same team of Israeli scientists led by Prof. Shai Efrati has further explored these original findings, and while the results are interesting, the media hype and marketing surrounding those results is frankly ridiculous and entirely unwarranted.
Stem cells hold so much potential for regenerative medicine, it is understandable that so many people should be so impatient to see all that potential realized. But people, the desperately ill among them, need to recognize that stem cells aren’t talismans. In unregulated clinical settings, stem cells can be worthless or even harmful. That’s the bad news. The good news is that stem cells are giving up their profound but decidedly unmagical secrets.
What stem cells lose in mystery, they gain in practicality. They are to be seen as manageable biological units that can, given the right preparation, perform myriad therapeutic applications, less as miracle workers and more as drudges that accept reprogramming and subsequently perform their assigned tasks. They may also sacrifice some of their protean identity, turning into cells that are less stemmy but more effective (and safer) as therapeutic agents. Stemminess may even by bypassed completely, as when cells of one type are directly transdifferentiated into cells of another type.
Even as the preparation of stem cell therapeutics becomes more sophisticated, it is becoming more streamlined, more industrialized. Helping to advance both trends—greater refinement, greater manufacturability—is a new generation of biotech startups. Several of these startups are described in this article. By commercializing the latest stem cell technologies, these startups mean to add to the list of FDA-approved cell-based treatments.
The replacement of lost neurons is a holy grail for neuroscience. A new promising approach is the conversion of glial cells into new neurons. Improving the efficiency of this conversion or reprogramming after brain injury is an important step towards developing reliable regenerative medicine therapies. Researchers at Helmholtz Zentrum München and Ludwig Maximilians University Munich (LMU) have identified a hurdle towards an efficient conversion: the cell metabolism. By expressing neuron-enriched mitochondrial proteins at an early stage of the direct reprogramming process, the researchers achieved a four times higher conversion rate and simultaneously increased the speed of reprogramming.
Neurons (nerve cells) have very important functions in the brain such as information processing. Many brain diseases, injuries and neurodegenerative processes, are characterized by the loss of neurons that are not replaced. Approaches in regenerative medicine therefore aim to reconstitute the neurons by transplantation, stem cell differentiation or direct conversion of endogenous non-neuronal cell types into functional neurons.
Researchers at Helmholtz Zentrum München and LMU are pioneering the field of direct conversion of glial cells into neurons which they have originally discovered. Glia are the most abundant cell type in the brain and can proliferate upon injury. Currently, researchers are able to convert glia cells into neurons — but during the process many cells die. This means that only few glial cells convert into functional nerve cells, making the process inefficient.