 Do we have to age? Well The Guardian has started 2021 with a new interview of Andrew Steele, author of Ageless, The New Science of Getting Older Without Getting Old. Steele believes longevity research should become mainstream, and so do we. 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, Andrew Steele believes we will be hopelessly unlucky if scientists don't make a longevity breakthrough within 10 years, given how many human trials are already in progress or upcoming. And although these breakthroughs probably won't result in treatments that extend our lives by 100 years, Steele believes they will give us enough extra time to ensure we're alive for subsequent breakthroughs, treatments, and additions in Lifespan, and so on. Steele states, quote, ultimately, I don't want this because I want to have a load of 150 year olds looking like 20 year olds. I want it because those 150 year olds won't have cancer, they won't have heart disease, they won't be struggling with arthritis, end quote. Steele also addresses the very common concern that increased lifespan will lead to overpopulation. And we've got a series about increased lifespan and overpopulation coming up here soon on X10. Moving on, Vicetin may be useful in treating pulmonary fibrosis. Vicetin is a flavonoid found in plants and known to have antioxidant properties. Vicetin is also known to be an anti-inflammatory and is shown promises as a synolytic, which is a compound that encourages aged or damaged senescent cells to destroy themselves rather than lingering in the body and contributing to inflammation, which is the chronic age-related inflammation that is associated with a wide range of age-related diseases. In a new study, researchers showed that Vicetin also had an anti-inflammatory effect in fibrotic mice and reduced senescence and epithelial cells. This brings Vicetin one step closer to being tested as a treatment for fibrosis in humans. 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. For our next story, stem cell growth factors were used to treat Alzheimer's in aged mice. Mice don't develop Alzheimer's, so research uses mice genetically engineered to have the disease. However, these mice usually get Alzheimer's earlier in their life than humans would. So researchers at Sunny Upstate Medical University in Syracuse have repeated experiments using stem cell growth factors to treat Alzheimer's. But this time, the researchers used older mice instead of the normal younger Alzheimer's model mice. The researchers found a dramatic reduction in beta-amyloid deposits and in the size of tau tangles in mice treated with the stem cell factors. While this is not a dramatic development, it's good to see that the results hold up in older mice. It's also encouraging and important that researchers are carrying out studies in older mice despite the higher cost of housing the animals for longer and the pressure to publish quickly. Moving on, a cause of genomic instability has now been discovered. Double-stranded breaks in DNA are dangerous to cells and play a role in aging. A new study from Universitat Autonoma de Barcelona in Spain has shown that a molecular marker known as 5-3-B-P-1 is important for aged cells to detect and repair double-stranded breaks. The researchers irradiated cell cultures and found that the breaks in older cells had less 5-3-B-P-1 than those in younger cells. The researchers think this is probably because it isn't being recruited to the breaks as well as in younger cells. We don't know if these findings will hold in other cell types or DNA damage from different sources. Nevertheless, these findings give us a glimpse of one more piece of the process of repairing DNA damage. For our final story, MYSM-1 prolongs lifespan by regulating DNA repair. The MYSM-1 gene was recently found to be more strongly expressed following DNA damage and that a lack of MYSM-1 decreased lifespan in mice. Now, a new study from Wuhan University in China has shown that MYSM-1 is involved in regulating the repair of DNA damage during aging. The researchers also found that mice treated with MYSM-1 lived longer and showed fewer signs of aging than control mice. The mice didn't lose their hair, their organs were in better shape, and they didn't develop the age behaviors seen in the control mice. So hurrah for the mice! Let's hope that science like this moves into human trials soon. That's all the news for this video. Thanks for watching on our new X-10 channel. 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 let others know about our new X-10 channel, and make sure you're subscribed with the bell turned all notifications to ensure that you don't miss any videos. Are there any recent life extension stories that you're excited about that we haven't included in one of our videos? Also, which of these 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.