 The gene editing tool CRISPR has made headlines in recent years for its potential to eliminate disease, enhance human capabilities, and even create designer babies. Now, new research suggests that CRISPR techniques may also be used to reprogram cells to a younger state. We'll have this story and more on this episode of Lifespan News. Welcome to Lifespan News on X10, your source for longevity science updates. I'm your host, Ryan O'Shea. As always, we encourage you to check the links below for more on these stories. Continuing with our first story, scientists have developed a new technique using CRISPR that makes it possible to switch genes on and off with greater precision and ease. All cells have the same genome, but not all genes are switched on or expressed in all cells. The epigenome, which you can think of as genetic switches, is different for different cell types, and it determines which genes are expressed and which aren't. As we age, our epigenome changes in unwanted ways, switching on or off the wrong genes. Scientists have been able to reset the epigenome in cells to a younger state for a while now, thanks to exposure to four chemicals known as Yamanaka factors. However, this process is complicated, requires precise timing, and is indirect in that exposure to Yamanaka factors pushes cells to use their internal machinery to reset the epigenome. The new technique, based on the popular CRISPR-Cas9 gene editing tool, enables directly changing the epigenome of cells, switching genes on or off at will. More specifically, the new technique allows to methylate or demethylate specific portions of the genome using single guide RNA. In experiments, the technique performed very well, with over 80% of the targeted genes remaining silenced 50 days after the application. At the moment, this method is only useful in laboratory cells, and it's going to be a while before it might be used to reset the epigenetic makeup of aged people to a younger state, but it's still a breakthrough that will facilitate aging research. For our next story, scientists have managed to reprogram a type of brain cell, known as astrocytes, to become healthy neurons. The ability to regenerate tissue in mammals is rather poor, particularly in the brain, which can regenerate only in certain areas and only to a certain extent. Cellular reprogramming can be used to turn existing cells into cells of different types, which can be especially useful for the treatment of cognitive decline. Astrocytes are close relatives of neurons and are much more abundant in the brain. Their similarity makes them ideal candidates for conversion into neurons. The authors of the study used an experimental drug cocktail to see if it was able to turn astrocytes into neurons, both in vitro and in vivo. The experiment was performed on live adult mice, and after two weeks of treatment, the researchers were able to confirm that a considerable amount of new neurons had been formed, though it varied depending on brain regions. According to their analysis, the newly formed neurons were fully functional and fully integrated into the existing brains. As usual, the path from this experiment to the clinic will likely be long, but one day it might be possible to use this technique to help people with brain damage or cognitive decline. By the way, Lifespan News is released every Tuesday at noon Eastern time, while our other X-10 science and advocacy shows are released every other Monday, also at noon Eastern. We encourage you to subscribe to our X-10 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. In a recent episode of Lifespan News, we discussed how the dog aging project is studying aging in pet dogs, which may lead to treatments to slow it down or reverse it. Now a new video has just been released by Science to Save the World, which dives into this topic further and features interviews with the scientists leading this initiative. Make sure to visit their YouTube and Facebook page to watch part one, and subscribe so you don't miss part two. Moving on. A recently published manuscript reports a 20% increase in the lifespan of middle-aged mice following a treatment of recombinant serum albumin. Serum albumin, a component of vertebrate blood plasma produced by the liver, is the most common blood protein in mammals. Because aging affects circulating blood factors, researchers hypothesize that diluting the damaged serum albumin in middle-aged mice might extend their lifespan. To test this, they gave 12 month old mice serum albumin injections every three weeks. This resulted in a 17.6% increase in female lifespan and a 20.3% increase in male lifespan. The treatment also improved grip strength and performance on a maze test. The researchers also reported that the treated mice had glossier and thicker fur than the control group. These results indicate that fresh albumin increases the lifespan of mice, supporting the notion that longevity can be promoted by restoring lost beneficial factors in aged blood or by reducing the harmful factors. However, the exact mechanism behind the success of this treatment remains unclear. It's also important to note that this reporting is based on a pre-print manuscript, so these findings have not yet been peer reviewed. A new study suggests that the longevity benefits of hypoxia may be a result of the suppression of the inflammatory senescence-associated secretory phenotype, or SAS. In cell cultures, hyperoxygenation accelerates cellular senescence. An extreme hypoxia has been found to reduce senescence and even put cells into an inactive state. In the new study, researchers compared cell cultures grown under normal oxygen levels to those grown under mild hypoxic conditions. They found that expression and secretion of multiple pro-inflammatory markers characteristic of the SAS were dramatically increased in the hypoxic condition, suggesting that mild hypoxia may limit the most negative effects of cellular senescence. Inhibiting HIF-1 alpha, a factor known to sense low oxygen conditions was not sufficient to raise SAS levels in hypoxic cells, suggesting that other mechanisms were at play. The team then turned to mTOR, which was strongly expressed in normaloxic conditions, but absent in the hypoxic non-senescent cells. Activation of mTOR restored the SASP in cells cultured under hypoxic conditions. The same was found for AMPK, indicating that the AMPK-MTOR pathway may mediate the link between hypoxia and SASP. This study will be useful in trying to understand whether and how hypoxia is beneficial. The findings might also be useful in research on other pathways. That's all for this video, but before you go, there are a few quick, free, and simple things that you can do to help us solve the problem of aging. First, make sure you like this video, and make sure you're subscribed with the bell icon turned to all notifications. Then you can share this video on your social media. This helps us spread the word and let more people know about the importance of life extension science. Is there a recent life extension story that we didn't cover that you think we should have, and what was your favorite story from this week's video? Let us know in the comments below. We really appreciate it, and we look forward to seeing you next week on Lifespan News.