 2021 has just begun and hopefully it will be better than 2020 in many ways. There's lots of longevity news and events to look forward to in 2021. For starters, billionaire Jim Mellon stated in December 2020 that his longevity portfolio company, Juvenessence, was scheduled to have its initial public offering sometime in mid 2021. So we'll start off with the top things to watch in the longevity industry in 2021. We'll have this story and more 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. For our first story, Longevity Market Cap shares their top 10 things to watch in the longevity industry in 2021. Juvenessence has raised $162 million in venture funding, which includes their most recent $100 million Series B. Juvenessence has a post-money valuation of $500 million, according to Craft.co. Hopefully funding for aging research will continue to increase in 2021. Dr. Kristen Fortney's AI computational drug discovery company, BioAge, recently closed a $90 million Series C round led by famous Silicon Valley venture capitalist firm Andreessen Horowitz. BioAge will use the funds to initiate Phase 2 clinical trials this year. BioAge uses artificial intelligence and machine learning and systems biology models to mine multi-omics, patient data sets, and identify existing drugs that are likely to treat age related disease. Dr. Nir Barzilia, professor of genetics at Albert Einstein College of Medicine, an organizer of the TAME Metformin Longevity Trial, spoke with the Forsyte Institute on their YouTube channel published on November 30th, 2020. In the video, Nir mentioned that an unnamed individual was in the process of setting up a longevity foundation that would spend $1 billion a year on aging research and biotech around the world, and that organization will also fund TAME. Nir said he knows the guy who will be the president or CEO of this mysterious organization, and the foundation will be announced in January of 2021. Nir will be on the scientific advisory board of this organization. This, of course, is a big deal, not just from a funding standpoint, but also from the publicity and change in social zeitgeist it will cause. More studies and clinical trials should be publishing their result this year, and we can expect more exciting news about AI applied to biology and drug discovery. If you want to find out more about what you can expect in longevity in 2021, then check the description below for a link to a detailed list on longevity market cap. For our next story, Cinelytics Reduce Gut Inflation in Mice. A recent study currently in preprint explored the long-term effects of a known Cinelytic drug combo, dacetinib and coercitin, also known as D plus Q. The two drugs were first tested in mice years ago in a Mayo Clinic study, and they were found to be able to destroy senescent cells. If you're not familiar with them, senescent cells are cells that no longer replicate, but aren't disposed of either, and contribute to age-related chronic inflammation, also known as inflamaging. The new study assessed the long-term effects of D plus Q in terms of gut microbiome composition, senescent cell populations, and inflammation. Analysis of senescence biomarkers revealed that animals that were given D plus Q had reduced senescent cell activity or presence in their intestinal walls compared to control animals. Other analysis showed a reduction of inflammation biomarkers in treated mice. The study also found a correlation between inflammation and the presence of specific gut bacteria. The researchers suggest that optimized senolytic regimens might improve health in older subjects, as this kind of treatment appears to reduce senescence of the intestine, as well as inflammation and microbial imbalance. We encourage you to subscribe to our new X10 YouTube channel. Once you're subscribed, be sure to click the notification bell and select all notifications to ensure you don't miss any videos. Now, back to the news. Arterial stiffening correlates with cognitive decline. Are blood vessels stiffen with age? Many factors seem to contribute to this phenomenon, such as the formation of unwanted cross-links within cellular scaffolding and the increasing presence of senescent cells. Blood vessel stiffness, especially in large arteries such as the aorta, has long been associated with heart disease. But researchers suspect it might also be associated with dementia, so a new study sought to explore this connection by studying over 500 older people. Patients had their aortic stiffness measured at age 64 and then again at age 68. Shortly after the second measurement, patients took cognitive tests and brain MRIs to examine the size, connections, and blood supply in different regions of their brains. The researchers observed that the patients with the faster rate of aortic stiffness had also lower blood flow and poorer markers of brain connectivity in different brain areas. The study also found that worse memory performance seemed to be more linked to the first aortic stiffness measurement rather than the second. The researchers noted that while this was a large study, their sample wasn't very diversified, as most participants were male, so it would be necessary to conduct similar studies on more representative samples to draw more accurate conclusions. For our next story, exercise is found to have anti-synescence effect. Exercise is already known to be a very powerful anti-aging tool. It helps maintain a healthy weight, glucose levels, and blood pressure among others. A recent review suggests that one of the mechanisms behind the benefits of exercise might be that it helps reduce senescent cells. The review looked into 21 different studies conducted on humans, animals, or both. Human participants range from athletes to casual exercisers and included healthy and ill people of different age groups. Animal groups exhibited similar variety and some of the animal studies included force exercise too. 16 out of the 21 studies demonstrated that physically active people are less burdened by senescent cells than sedentary people. Animal studies too showed that exercising reduces senescent cells, but interestingly, this didn't seem to be true in the case of forced or excessive exercise, which led to increased senescence. So while we wait for effective pharmacological interventions against cellular senescence, hating the gym is still worth it. For our final story, senescent cells recruit sympathetic nerves. A study published in Frontiers of Aging Neuroscience showed that senescent cells secrete a compound that favors the growth of sympathetic nerves, which play a key role in our fight-or-flight response, elevating blood pressure, suppressing digestion, and making us start to sweat when necessary, among other things. Overactivity of the sympathetic nervous system appears to be involved in many age-related disorders, and it's been observed that many tumor types exhibit a high density of sympathetic nerve fibers, or SNF. To investigate the role of senescent cells in sympathetic nervous system overactivity, a Chinese study examined two models of aging, tissue from naturally aged mice and human tumor tissue, and showed that SNF was higher compared to normal tissue. The researchers also found signs of senescent cell activity alongside SNFs, so the researchers proceeded to inhibit the activity and proliferation of SNF using drugs that act on them directly, and observed improvements, for example, better cognition or reduction of liver disease in mice. The researchers hypothesized that senescent cells might promote SNF proliferation through the secretion of SASP, which is a well-known mix of pro-inflammatory chemicals typical of senescent cells. So to test this hypothesis, the researchers looked at a cell culture that included a type of SNF in fibroblast cells. The researchers then induced senescence in fibroblasts in different ways and found that senescent fibroblasts indeed induce SNF growth, unlike young fibroblasts. The researchers also tested their hypothesis in mice by surgically inducing osteoarthritis, which is an inflammatory disease in which senescent cells are known to be involved. This induced an increase of SNF in the joints of the mice. A senolytic treatment reduced both senescent cells and SNS. The researchers suspect that NETRIN-1, which is one of the factors in SASP, might be the main culprit. Blocking NETRIN-1 completely seems to have prevented the same SFN growth observed in the previous experiments. However, the mechanisms by which SNFs contribute to age-related decline are largely unexplored and may provide insights into how to intervene in these processes with fewer side effects. This study represents an important step in connecting these concepts for the benefit of human health. 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 like this video, share this video on social media to help us spread the word about our new X10 channel, and make sure 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 recent 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.