 Welcome back to the third annual Vail Scientific Summit. Recently I chatted with Dr. Laura Niedernhofer and her husband, Paul Robbins, both with the Scripps Research Institute. And I chatted with them about what it's like to be a married couple working in the world of regenerative medicine and anti-aging. I'll let you start. Go ahead. Yeah. So we're trying to understand two aspects of aging. One is the basic biology of what drives aging. Why is it that we age at the rate we do? And then secondly, we're trying to develop ways to intervene with that process so that we can actually slow down the aging process and potentially even reverse that. And we've been doing this all in mouse models, but the goal now is to be moving this towards the clinic. So, and the real idea behind that is aging is of course the number one risk factor for virtually every chronic degenerative disease and cancer as well. So if we could therapeutically target the aging process itself, then we could really attenuate or prevent all of these diseases at once. So that's the long-term goal. So it's been a very complementary relationship in this because we both have our strengths and weaknesses in science, both have our strengths and weaknesses in our private lives. And so it's actually been just wonderful. We spend 24 hours a day together. We're usually at work seven days a week. We're at home. We're talking about our research and directions we're going. I'm much more the 30-foot-thousand-view guy, and she's the one who deals with the details, both at work and at home. And that has led to a very successful partnership all the way around. Yeah, great. It's been great. And what's really fun, too, is I think we both entered the aging field at the same time. So this was about 10, 12 years ago. And it certainly wasn't on anybody's radar screen at that time. So I feel like we got in on the ground floor, although we were already standing on the shoulders of giants. But we came from very different perspectives. So Paul has a strong background in autoimmune diseases, understanding immunology, the orthopedic background. And I came from understanding damage that could drive aging and how we get rid of it in our cells. So it has been extremely complementary. Yeah, so one of the things that we've shown over the last five years, and we being more of myself but others in the field, is that as we age, we acquire damaged cells in our body. And that these damaged cells, which are termed senescent cells, actually are bad. They release bad factors that not only age locally a tissue, but they age the whole body systemically. So one of the things we're working on is to develop ways we could kill these bad cells specifically. And so we've developed drugs that will actually go in and target and then kill these bad cells. And then mice and then clinical trials, which are starting, the periods of clearing these cells does extend healthy aging. And we're hopeful that this will lead to a new paradigm of how we treat aging in humans. So I would just add to that our job at Scripps, I think, is to develop a drug pipeline. So what's really holding back the field of aging right now is the FDA says, well, how are you going to treat aging because it's not a disease? So we've had to create with a lot of colleagues a pathway that we could actually get these drugs into people. So the first clinical trial designed to treat aging has been designed and approved by the Food and Drug Administration. So that'll be initiated this year. So we want to have a very robust pipeline of drugs that can go in right behind this proof of principle clinical trial. So we've got these synolytics that Paul was talking about. We also have drugs that can target pathways that sort of get activated and angry when you have damage. And so I think we have kind of a pretty robust panel of drugs and thought processes about how we're going to slow aging once we're allowed to try it. Right. So I started off working in muscle skeletal diseases. So looking at osteoarthritis, rheumatoid arthritis, muscle wasting, even work in cystic fibrosis. And one of the things I realized after spending 15 or 20 years working on these different diseases, isolated diseases, is that the same mechanisms, the same pathways were driving each one of these diseases. So a single drug would work in multiple models of disease. And we started to realize, well, the driving force behind all these diseases were actually processes that drove aging. And so a new concept that came out the last five or 10 years is a concept of geroscience, which is that you treat the root cause of disease, and that root cause of disease is aging. So by slowing aging, you could either prevent onset or delay onset of a whole myriad of age-related conditions. And so it was like an aha moment. It's like, what am I doing studying visual diseases? I'll study the underlying cause of every one of these diseases. But I'd add that the honest answer is turning 50. And you realize everything that comes with it. But, and then the other thing is kind of being the geeky little kids that we all were when we went into research, medicine, we wanted to change the world. And we wanted to have an impact that would be translated to people. And right now, aging is the number one biomedical problem on this planet without question. So it's being equated to when we discovered sanitation and penicillin. And all of a sudden people, their life spans doubled basically because they weren't dying of infectious diseases as children. And so aging, now we have an aging population instead of young sick children. So we've really got to tackle this. Yeah. So we try not to talk about lifespan because the goal is not to make people live longer, is to make them live healthier. So we're trying to compress the period of morbidity and the life period when everything starts to fail. You like to be healthy until you're on the golf course and have a heart attack at the age of 100. So we're not trying to extend lifespan. Now, if you extend health span, one of the benefits may be that you'll live longer. But that's not the end point that we're striving towards. It's healthier living. In fact, the way they articulate it for the clinical trials is it's all about reducing, as Paul said, these multiple morbidities with a single drug. But the side effect may be that you get a few more years of life. So not not the main goal, but just the side effect. If I could just just add because one of the end points of clinical trials for aging is actually cancer. So people never really think of cancer as an age related disease. But the highest risk factor for most cancers is aging. So this isn't just going to be osteoarthritis. It's going to be cardiovascular disease. This is actually going to be approaches to delay or even prevent certain types of cancer. So this will have wide ranging applications. When the focus of the summit has been on aging, because I think Johnny, who's the organizer of the meeting, is realizing that aging is an important component of many of the things he's working on. So he's he drank the Kool-Aid and has been convinced that this should be a focus because many researchers have spent their careers doing analysis in young mice. It's just easy or or young animals or but yet what the people were treating in the clinic are usually older. So I think everybody has started to realize we have to be looking at what goes on with aging. Luckily, many people at this symposium are really collaborating with and those who are not, I think, will leave here with new collaborations and new directions. So it's been a very exciting symposium. When I would add to that, aging is complicated. I mean, it really affects every organ system. And there's no one scientist who can master that big of a problem. So it's great to meet face to face with people who are dealing with bone or muscle or cartilage, all of which are affected with aging. So then we can share our expertise and say, hey, shouldn't you be measuring this and could you help me measure that? So I have to say this summit has been really valuable to me because I've met new colleagues that will change the course of my research. So I've got a new collaborator to work on disc degeneration, another one to work on bone and then exercise physiology. So it's been very exciting. Yeah, because the unique aspect of this symposium is is bringing clinicians, the top clinicians together with top basic researchers. And that doesn't usually happen. And so this interface between basic science and clinical science, it's always been the Valley of Death and research. So we treat mice, but then never makes into humans. And so the value of this symposium is bringing these two groups together. And then hopefully continuing to work together, not just me and Vale for four days, but continuous, we leave Vale to continue to collaborate. So it's a very exciting time.