 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 health span and lifespan. Can a new startup 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 startup 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% of them cannot be degraded in any way and wind up contributing to neurodegenerative diseases in other conditions. Celeris's 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 in R42 Group to develop their platform, Celeris One. This platform will consist of three different modules, Hades, Xanthos, and Hephaestos, each focused on different stages of the drug discovery process. Celeris hopes to attract the interest 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 USAG1 gene can stimulate tooth growth and 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 USAG1 gene. Previous studies had shown that suppression of USAG1 gene benefits tooth growth, but the team wanted to see to what extent. To suppress USAG1, the scientists tried different monoclonal antibodies for the gene and 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. By the way, Lifespan News is released every Tuesday at noon Eastern time, while our other science and advocacy X10 videos are released every other Monday also at noon Eastern time. We encourage you to subscribe to our X10 YouTube channel. Once you subscribe, be sure to click the notification bell and select all notifications to ensure you don't miss any videos. Now, back to the news. Scientists grow human muscles and 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 describe the 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 and 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 blastomers 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 tissues 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 hoped that in the next three to five years, it might be possible to start clinical trials of pig-grown human tissue transplants to help people who need them. Moving on, NAD plus 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 plus supplementation. NAD plus 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 AT. Patients who suffer from AT experience premature aging-like symptoms such as cognitive decline, motor dysfunction, immunodeficiency, cancer predisposition, and more. Researchers examined tissues from patients of AT and discovered elevated levels of cellular senescence and mitochondrial dysfunction. AT 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 plus, so this eventually leads to a steep decline in NAD plus that triggers the symptoms observed in AT patients. Therefore, NAD plus depletion isn't an upstream cause of AT, but the researchers hypothesized that targeting it may lead to symptom alleviation, which is exactly what they observed in the mice in the experiment. Using a NAD plus precursor known as nicotinamide riboside or NR, the researchers managed to replenish AT mice NAD plus 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 plus might be bad and that it's too early to tell whether NAD plus 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 therapeutic 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 hoped that depletion of SETDB1 may one day be used as a therapeutic tool for this and other types of cancer. That's all the news for this video. Before you go, there's a few quick, free, and simple things that you can do to help us solve the human aging problem. If you haven't already, please make sure to like this video, share this video on your social media, please make sure that you're subscribed with the bell turned to all notifications to ensure you don't miss any videos. Is there a recent life extension story that you think we should have included in one of our videos but haven't yet? And which of the stories from this video excited you the most? Let us know what you think in the comments below. We really appreciate it and we look forward to seeing you in the next video, at least as healthy as you are now.