 Why does our hair turn gray? And are there any current solutions for gray hair? Well, Lifespan.io has recently interviewed University of Alabama Birmingham professor Melissa Harris on the problem of graying hair and possible solutions to it. 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. Continuing with our first story, in her interview, Professor Harris explained that graying hair is thought to follow from the loss of specific stem cells called melanocytes, which are responsible for the production of hair and skin pigment. A reason why scientists have taken on this problem is that hair grain is an accessible easy to check marker of stem cell dysfunction. Making it easier to see if therapies are having an impact. Unfortunately, though, at the current time, there doesn't seem to be any treatment available to repigment hair, although different studies have observed hair repigmentation as an unexpected side effect of unrelated treatments, inducing researchers to suspect that hair discoloration may be reversible. In the interview, Dr. Harris also explained how research into melanocyte dysfunction may improve our understanding of stem cell dysfunction in general. Dr. Harris also said results of recent mouse studies on hair loss and repigmentation are promising and with some luck, we might see commercial applications in humans soon. For our next story, rapamycin is not a caloric restriction mimetic. Rapamycin and caloric restriction are two of the most reliable lifespan increasing interventions. Over the past two decades, a hypothesis has emerged that rapamycin is effectively a substitute for caloric restriction. Now, a team of researchers in the Netherlands used progeroid mice to investigate whether rapamycin really is a caloric restriction mimetic. Young progeroid mice fed rapamycin had no increase in lifespan. The researchers repeated the experiment in older mice and still found no increase. Likewise, varying the rapamycin dosage didn't lead to longer or shorter lifespan in these mice. The researchers also evaluated the health of the liver, vascular system, and nervous system in these mice and found no improvement. Basically, although caloric restriction clearly increases their lifespan, rapamycin seems to have no effect. So it seems like rapamycin and caloric restriction affect lifespan via different mechanisms. So this is bad news in terms of having a substitute for caloric restriction, but good news in that we now have two different reliable interventions which we can compare and investigate. By the way, lifespan news is released every Tuesday at noon Eastern time while our other X-10 science and advocacy videos are released every other Thursday at noon Eastern time. Our next video on X-10 will be Thursday, February 4th, 2021 and the topic is DNA methylation. We encourage you to subscribe to our new 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. Now, back to the news. A study in rats suggests that glucosamine could be a caloric restriction mimetic. Glucosamine is a polysaccharide that naturally occurs in cartilaginous joint tissues and is involved in protein and lipid synthesis. Glucosamine is also present in other tissues such as skin, nails, bones, and ligaments. Sunovial fluid contains glucosamine and occupies the space between joints, helping to reduce the friction of joint surfaces. Glucosamine is commonly taken as a supplement to help with the joint pain and inflammation associated with aging. Glucosamers gave regular doses of glucosamine to rats and then tracked various biomarkers. The treatment led to an increase in reactive oxygen species for ROS in both young and accelerated aging rats. The treatment also led to an increase in various antioxidants. ROS are reactive molecules and free radicals derived from oxygen and while ROS do have some beneficial uses such as being used by immune cells as a component of the killing response to combat microbial invasion, ROS are also very harmful to cells. Free radicals each possess an unpaired electron making them highly reactive and thus able to damage all macromolecules including lipids, proteins, and nucleic acids. The researchers believe that treatment causes a transient increase in ROS which then leads to a protective response, a process known as mitahormesis. So keep in mind that these results are of course in rats. But the idea that similar effects may occur in humans taking glucosamine is not beyond the realm of possibility. For our next story, synelytics alleviate age-related cognitive decline. A new study by a team of researchers including Dr. James Kirkland of Mayo Clinic tested the effects of whole body senescent cell pruning in mice. In this study, the researchers used mice engineered so that their senescent cells would be destroyed upon exposure to a specific trigger drug. The scientists examined the brains of young and old mice and observed an age-dependent increase in senescent cells. The researchers then went on to administer either the trigger drug or the cancer drug disatinib and the dietary supplement coercitin, which is a known synelitic combination called D plus Q. The researchers observed that both treatments reduced the number of senescent cells in a specific brain cell population, as well as the secretion of SASP, a pro-inflammatory chemical secreted by senescent cells. Additionally, both treatments appeared to improve the cognitive abilities of the mice. These findings suggest that an effective senolytic treatment could improve brain health and reduce age-related cognitive decline. So while this research was of course in mice, there are multiple senolytic drugs poised to enter human trials in 2021. For our final story, scientists published a blueprint to apply artificial intelligence to extend human longevity. A recent comment paper by Dr. Alex Zhavorankov of Deep Longevity argues that it's time for AI tools such as deep aging clocks or DAC to become part of physician's toolkits. The paper also argues that the employment of AI technology to the field of longevity medicine will facilitate the discovery of new, personalized drugs and drug targets tailored to specific individuals. Zhavorankov advocates for the cooperation of clinicians, geroscientists and AI researchers to gradually bring AI-based experimental longevity medicine to the clinic. So as with all our stories, if you want to learn more, make sure you check the description below for links to these stories. 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 you like this video. Share this video on your social media. 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 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.