One startup company is repurposing the gene-editing tool.
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Category: biotech/medical – Page 2,635
The link between inflammation, cellular senescence, aging, and cancer is a complex relationship, but a new study sheds light on how these four interact.
The light and dark side of inflammation and cellular senescence
Cellular senescence is a protective mechanism that helps us to stay healthy and avoid cancer by removing damaged and aged cells from the cell cycle while preventing them from creating damaged copies of themselves. Senescent cells are disposed of via a self-destruct process known as apoptosis.
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By scanning the brains of healthy volunteers, researchers at the National Institutes of Health saw the first, long-sought evidence that our brains may drain some waste out through lymphatic vessels, the body’s sewer system. The results further suggest the vessels could act as a pipeline between the brain and the immune system.
Dr. Daniel S. Reich, Ph.D., M.D., discusses how his team discovered that our brains may drain waste through lymphatic vessels, the body’s sewer system.
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Whenever the topic of increasing human lifespan is discussed the concern is sometimes raised that a longer life would mean a life spent frail and decrepit. This is sometimes known as the Tithonus error and shows a fundamental misunderstanding of the aims of rejuvenation biotechnology. The concern is based on the ancient Greek myth of Tithonus which might be thought of as a cautionary tale warning seekers of an eternal life of its alleged inherent dangers.
The myth of Tithonus in brief
Tithonus, the story goes, was a mere mortal who was in love with Eos, the beautiful titan of the dawn. His feelings were requited, but, unfortunately, their idyll was not destined to last. Being a titan, Eos was also a deity and thus immortal, unlike Tithonus, who one day would die of old age if not of some other cause. Eos thus turned to Zeus and asked him to make Tithonus immortal as well. Zeus granted Eos’ wish, but even this did not solve the two lovers’ problem; the father of the gods had granted Tithonus immortality, not eternal youth.
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End Aging Now
Posted in biotech/medical, life extension
As we age, the thymus begins to shrink, and fewer numbers of T cells are created and trained to fight. This structural decay of the thymus is one of the main reasons why we become increasingly vulnerable to infectious diseases, such as influenza and pneumonia. The other reason is immune cells becoming senescent.
So, what can we do about it? Check out our new exclusive interview and find out.
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As we age, the thymus begins to shrink, and fewer numbers of T cells are created and trained to fight. This structural decay of the thymus is one of the main reasons why we become increasingly vulnerable to infectious diseases, such as influenza and pneumonia. The other reason is immune cells becoming senescent.
There are a number of possible solutions to this problem. Firstly, engineering new healthy and youthful thymic tissue might help to restore the immune system, and indeed a number of groups are working towards this.
Secondly, some researchers are focused on encouraging the aged thymus to regrow using various approaches, such as stem cell transplants, cellular reprogramming or chemical compounds. Dr. Greg Fahy is involved in researching this second approach, and we had the opportunity to speak to him about this work.
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For this new book, Jim and Al have spent a year sifting through the cutting-edge research, visiting laboratories and interviewing key opinion leaders in the field of life extension. https://www.juvenescence-book.com/
My guest today on Stuff That Interests Me is one of Britain’s most successful investors, Jim Mellon.
You’re going to live till your 120.
Jim explains why — a combination of new drugs, technologies and lifestyles. What are you going to do with all your time?
The next great investment trend will be around the fact that we are all going to love a lot longer. Find out more in the this fascinating interview.
(Phys.org)—A team of researchers from the University of California and the University of Tokyo has found a way to use the CRISPR gene editing technique that does not rely on a virus for delivery. In their paper published in the journal Nature Biomedical Engineering, the group describes the new technique, how well it works and improvements that need to be made to make it a viable gene editing tool.
CRISPR-Cas9 has been in the news a lot lately because it allows researchers to directly edit genes—either disabling unwanted parts or replacing them altogether. But despite many success stories, the technique still suffers from a major deficit that prevents it from being used as a true medical tool—it sometimes makes mistakes. Those mistakes can cause small or big problems for a host depending on what goes wrong. Prior research has suggested that the majority of mistakes are due to delivery problems, which means that a replacement for the virus part of the technique is required. In this new effort, the researchers report that they have discovered just a such a replacement, and it worked so well that it was able to repair a gene mutation in a Duchenne muscular dystrophy mouse model. The team has named the new technique CRISPR-Gold, because a gold nanoparticle was used to deliver the gene editing molecules instead of a virus.
The new package was created by modifying a bit of DNA to cause it to stick to a gold nanoparticle and then a Cas9 protein and also an RNA guide. The package was then coated with a polymer that served as a containment casing—one that also triggered endocytosis (a form of cell transport) and helped the molecules escape endosomes once inside the target cells. The molecules then set to work—the Cas9 cut the target DNA strand, the guide RNA showed what needed to be done and a DNA strand was placed where a mutation had existed. The result was a gene free of a mutation that causes Duchenne muscular dystrophy.
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Many of us have experienced the uphill struggle to control our weight as we get older. We cannot eat whatever we like and stay slim like when we were younger, our holiday indulgences refusing to go away. The battle of the bulge gets harder the older we get, and there was little we could do about it, but now science has come to the rescue and is starting to unravel the mystery of why we find it harder to lose weight as we get older.
A new study led by Professor Vishwa Deep Dixit at Yale University shows how both the nervous system and the immune system talk to each other and, in doing so, control metabolism and inflammation in the body[1]. This study sheds light on why older adults often find it difficult to burn stored belly fat, increasing the risk of a number of metabolic disorders.
Perhaps more intriguingly, the study also shows some potential approaches to targeting the problem, thus helping older adults to improve their metabolism, improve weight control and reduce the risk of metabolic disorders.
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