This week on Lifespan News, Brent Nally discusses how a new company aims to cut down longevity drug development down by years thanks to AI and deep learning. Meanwhile, scientists managed to regrow missing teeth in mice and to grow human muscle tissue in pig embryos. We also discussed a new means of stopping colorectal cancer from proliferating.
We all know that technology is rapidly improving and changing how we live. But we’re going to need even more technological breakthroughs to improve human maximum healthspan and lifespan. Can a new start-up cut longevity drugs development from 15 years to one? We’ll have this story plus four other stories in this episode of Lifespan News.
Welcome to Lifespan News on X10, your source for longevity science updates. I’m your host, Brent Nally. If you missed our last episode, then you can watch it by clicking the card above. We encourage you to check the description below for links to these stories.
Continuing with our first story, Celeris Therapeutics is an Austrian start-up aiming to accelerate the development of longevity drugs using artificial intelligence. The key factor that Celeris wants to focus on is the degradation of pathogenic proteins, which are one of the main drivers of age-related diseases. Currently, most of these proteins are undruggable: around 80 percent of them cannot be degraded in any way and wind up contributing to neurodegenerative diseases and other conditions. Celeris’ goal is an “end-to-end, automated, early-stage drug discovery pipeline” to discover new molecules to break down unwanted proteins. Celeris hopes to show that, thanks to deep learning, it may be possible to “achieve in one year what used to take 15 years of drug development time.” To this end, Celeris has recently secured 400,000 from Longevity Tech Fund and R42 Group to develop their platform, Celeris One. This platform will consist of three different modules, Hades, Xanthos, and Hephaistos, each focused on different stages of the drug discovery process. Celeris hopes to attract the interests of big pharma companies as early as summer 2021.
For our next story, there’s a new drug to regenerate lost teeth. A new study by Kyoto University and Fukui University scientists offers hope that regrowing teeth in adults may be possible. Their discovery shows that an antibody for the USAG-1 gene can stimulate tooth growth in mice suffering from a congenital condition that causes them to lack teeth. Scientists already knew that molecules such as BMP and Wnt signaling pathway are involved in tooth development, but they also are involved in other processes; for that reason, drugs that target them are normally avoided, as this could have body-wide side effects. So the authors of the study thought instead to target factors that are known to antagonize BMP and Wnt, one of them being the USAG-1 gene. Previous studies had shown that suppression of USAG-1 gene benefits tooth growth, but the team wanted to see to what extent. To suppress USAG-1, the scientists tried different monoclonal antibodies for the gene in mice. Most of them had serious side-effects, but one in particular showed more promise, as a single administration was enough to regenerate a whole tooth. Similar results were obtained in ferrets, and now the scientists plan to move on to pigs and dogs.
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Scientists grow human muscles in pig embryos for the first time. Oh man, I need to hit the gym. In a study published in the journal Nature Biomedical Engineering, scientists described a procedure to create human-pig chimeras that may facilitate muscle transplantation. Chimeras are organisms or tissues that contain at least two different sets of DNA; in particular, interspecies chimeras contain DNAs from different species. The authors of the study created human-pig chimeras with the hope that this may one day help make muscle transplantation easier. Unlike other organs, muscle tissue can’t be transplanted from deceased donors, and people whose muscles have been damaged beyond repair because of accidents or surgical removal of tumors can’t be treated, leading to lifelong disabilities. Previous studies had already shown that it’s possible to grow human organs in pig embryos, but this study was the first to show that it also could be done with muscle tissue. The researchers created pig embryos that lacked the gene to develop their normal muscle tissue; then, the researchers injected either pluripotent human stem cells or porcine blastomeres from a related species, so that the modified embryos would either grow human muscle tissue or muscle tissue of a porcine relative. Already between 20 and 27 days of incubation, it was possible to detect human muscle tissue in the human-pig embryos; pig embryos that carried muscle tissue from other porcine species developed into absolutely normal piglets too. The researchers made it clear that the human cells used were only located where muscle tissue should be, and that they didn’t migrate to the brain or reproductive areas of the pig, so there is no reason to worry about human-pig hybrids. The researchers also hope that in the next 3 to 5 years, it might be possible to start clinical trials of pig-grown, human tissue transplants to help people who need them.
Moving on, NAD+ eases symptoms of a premature aging disease in mice. Scientists managed to alleviate the symptoms of a rare, premature aging disorder in mice by using the coenzyme nicotinamide adenine dinucleotide, or NAD+, supplementation. NAD+ is a ubiquitous molecule that is employed in hundreds of different cellular processes, and its age-related decline is implicated in at least three hallmarks of aging. The disease focus of the paper is called ataxia-telangiectasia, or A-T. Patients who suffer from A-T experience premature aging-like symptoms, such as cognitive decline, motor dysfunction, immunodeficiency, cancer predisposition, and more. Researchers examined tissues from patients of A-T and discovered elevated levels of cellular senescence and mitochondrial dysfunction. A-T is known to be caused by a mutation in a gene that produces ATM kinase, which is a molecule playing a key role in DNA repair. The lack of ATM kinase prevents DNA repair from happening; this leads PARP1, which is another molecule involved in DNA repair, to constantly stick around for a repair job that never finishes. PARP1 uses up a lot of NAD+, so this eventually leads to a steep decline in NAD+ that triggers the symptoms observed in A-T patients. Therefore, NAD+ depletion isn’t an upstream cause of A-T; but the researchers hypothesised that targeting it may lead to symptom alleviation, which is exactly what they observed in the mice in the experiment. Using a NAD+ precursor known as nicotinamide riboside, or NR, the researchers managed to replenish A-T mice NAD+ levels and ameliorate their symptoms. However, in healthy control mice, especially young ones, NR treatment seemed to cause inflammation and DNA breakage, suggesting that too much NAD+ might be bad and that it’s too early to tell whether NAD+ supplementation in healthy young humans is advisable or not.
For our final story, a cell culture study demonstrated that forcing cancer cells to differentiate into somatic cells prevents their proliferation. One of the hallmarks of cancer is its uncontrolled division that allows it to grow and eventually spread throughout the body. However, like normal cells, cancer cells can be more or less differentiated, that is specialized in a particular type of tissue. While destruction of cancer cells is a typical therapeutical avenue, the authors of this study suggest it may be possible to stop cancer from proliferating by pushing cancer cells towards differentiation, thus making cancer cells closer to normal, somatic cells that do not divide further. So, to test their idea, the researchers examined colorectal cancer cells in a culture and identified five factors that would normally allow them to differentiate. The researchers also identified a factor, called SETDB1, to be an inhibitor of these five factors. By depleting SETDB1, the researchers managed to promote the five pro-differentiation factors in colorectal cancer organoids, which resulted in a markedly reduced ability of the cancer to spread, having been turned mostly into harmless tissue. The researchers hope that depletion of SETDB1 may one day be used as a therapeutic tool for this and other types of cancer.
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