← RealTalk MS
RealTalk MS
Episode 433: Our Most Important Conversations of 2025 with Dr. John Corboy, Dr. Mikael Simons, Dr. John DeLuca, and Dr. Stehen Krieger
00:43:16
Loading summary
Transcript75 lines
- [00:01]
A
I'm john strum, and this is real talk, mississippi. It's December 16th and we have a lot to talk about as the year draws to a close. I wanted to share some of the most compelling conversations that I've had over the past 12 months. And that's no easy task because I've had the honor of welcoming so many truly remarkable guests who were kind enough to join me each week. So I decided I would take a slightly different approach to choosing which of those conversations I would share with you by looking through the email that I received from the Real Talk Ms. Listener community over the past year to see which topics really connected with you. And so this week I'm sharing four conversations with some of the top Ms. Experts in the world addressing the topics that you told me were most important. One of the topics at the very top of that list is Aging NMS and last February at the Actrooms forum, I spoke with Dr. John Corboy, the principal investigator for Disco MS, which is the largest clinical trial to focus on one of the central questions related to Aging and Ms. Once someone hits the age of 60, can they discontinue their disease modifying therapy? In a moment, we'll hear my conversation with Dr. John Courboy. Dr. John Courboy founded the University of Colorado Ms. Center, which morphed into the Rocky Mountain Multiple Sclerosis center at the University of Colorado. He's also the principal investigator in the Disco Ms. Clinical trial, which was the largest clinical trial to focus on whether it makes sense for someone over the age of 55 or 60 to discontinue their disease modifying therapy. Welcome to the Actrooms Forum 2025 and welcome back to Real Talk Ms.
- [02:12]
B
Thanks John. I'm happy to be here and thanks for having me.
- [02:16]
A
As the population ages, we've seen a greater focus on the whole subject of Aging and Ms. How many people over the age of 55 are living with MS?
- [02:25]
B
A substantial number of people in the United States and around the world are living with multiple sclerosis who are 55 and older. The best data from a large demographic study was published several years ago suggests that of U.S. adults, 46% are 55 and older, and we have for many years just thought of Ms. As a young person's disease. But in reality there are many people who live long lives and are living longer lives. Now. The likelihood of dying early from your Ms. Is also diminishing. So people are living older and older. We're diagnosing older people with Ms. And just from a numbers point of view, it's almost half of people are 55 and older.
- [03:03]
A
So we're looking at somewhere in the neighborhood of half a million people.
- [03:06]
B
Somewhere in the neighborhood of half a million people. That same study I mentioned suggested up to a million people in the United States have Ms. That's the upper end. It could be as low as 700,000. But a substantial number, hundreds of thousands of people could be over the age of 55.
- [03:20]
A
Why are people with Ms. Living longer?
- [03:22]
B
They're living longer, I think because of a couple things. Number one, we're probably identifying people with relatively modest disease who don't have any substantial impact in terms of disability and dying young with their Ms. The second part, of course, is that we've developed effective therapies. And these effective therapies have reduced the likelihood that someone would develop progressive disability, diminished the severity of that progressive disability. And we also have just better ways to treat infections, better ICU care over time. It used to be in the old days that people would, for example, get blood clots in their leg and they would go up to their lungs, so called blood clots that would go up and pulmonary embolism, and they would die from that on a routine basis. Now we can recognize that much better. And we don't have that issue. And this is not a trivial issue for our patients because our patients, many of them are wheelchair bound, and that is potentially a risk factor for developing pulmonary mli.
- [04:15]
A
How does Ms. Change as people age?
- [04:18]
B
Ms. Changes functionally in many different ways as people age. So pathologically there are differences in the way the immune system is disrupted as people age. When people are younger, they have these highly inflammatory lesions with white blood cells leaving the periphery of their body, entering into their nervous system, causing these acute relapses. As they age, that becomes much less significant. And there's what's called compartmentalized inflammation and there's so called senescence of the immune system as well. And so all of those things result in clinical changes that we see with decreased relapses. And as I noted before, some significant component of people go on to have slow progression of disability, and that is much more prominent as people age. Radiographically, that's seen with people having less new active MRI scan lesions, but they still can have slowly expanding lesions, something recognized more recently. They can also have brain volume loss or shrinkage. When people are young, most of that shrinkage is due to Ms. As people age, most of the shrinkage they have is actually due to aging. And so what we can think of as Ms. In older People, when they have slow progression, it is taking Ms. And plopping it onto the back of aging, and the two together are not good. And so doing whatever we can before people get old to limit that would be extremely important. So in addition, what we see that's relevant to the Disco Ms. Study is that as people age, the benefit of these medicines seems to be more limited. That is, when people have these relapses, when they're younger, the medications are very effective. When people have slow progression of disability, the medicines are much less effective. So that's a big change. And that's what was partly what prompted us going in to do the Disco Ms. Study.
- [06:03]
A
As you mentioned a moment ago, as we age, things change. We physically change. And as people with Ms. Age, their Ms. Changes too. How challenging is it for a neurologist to sort of determine whether that patient in front of them, are those changes due to their Ms. Or are they due to the fact that they're simply aging?
- [06:26]
B
The question of what causes the problem as you age, is it Ms. Or something else? Is an incredibly important question because, number one, you would treat them very differently, and what you tell the patient will be very different. So the things that are very important over time are things related to vascular disease. So simple things, little white dots on brain scans can be due to Ms. Or they can be due to vascular disease or orthopedic problems, spine problems, hip problems, knee problems, those can absolutely affect your gait. So one of the main things that we have to do as physicians as people age is exactly what you alluded to, which is say, what the heck is causing this? And is this really something I have to pay attention to differently? You know, especially if somebody has some serious problem like increasing fatigue with shortness of breath, well, that could be congestive heart failure and not Ms. So we really have to become almost more like old fashioned doctors that took care of a lot of different things, not just the Ms. Whereas in young people, they mostly are pretty healthy. And we can focus almost exclusively on the Ms. And so it's a mind shift for us when we see an older patient to think about all the other things.
- [07:34]
A
I want to circle back to something you said regarding what you learned in the Disco Ms. Study about some of the medicines not being as useful to the patient as they were when they were younger. Given that, what's the conversation that that patient should be having with their neurologist after they're celebrating their 60th, 61st birthday?
- [07:57]
B
So the main conversation that we should have with our patients over Time, especially as they go over age 60, assuming they've been diagn with Ms. When they're 25 or 30, which is not uncommon, is do I need to continue this therapy? And the decision's always going to be based on the same thing. What are the potential benefits of the medication? What are the potential risks of the medication? What are the potential costs of the medication? And if I go off, how does that change? What does it change with regard to my risk of having new disease activity or worsened disease activity, and how do I balance those risks and benefits out? And if for that individual person, the risks and benefits say I should really stay on my medication, that's okay, but you should have that discussion so you have the best information available that would then say what's good for you? And everyone is going to be different in that regard. Everyone views risk differently. And so we can't say there's one thing, one size fits all, and everybody should do the same thing. The reality is that there's, first of all, no one size in general, but it's definitely not going to fit everybody with regard to how they understand risk and what their comfort level is and what their family's comfort level is. I can tell you that one of the main reasons we had difficulty enrolling people into the Disco Ms. Study was that many people are quite uncomfortable at the idea of going off their medication. But importantly, so are their spouses. And spouses and family members have an oversized influence on people when they make decisions, because like most people, we like to get help making complex decisions, and the spouses and family members play a very large role.
- [09:37]
A
You know, we started our conversation talking about the fact that people with Ms. Are living longer. Have you noticed that people are being diagnosed with Ms. At a later age than perhaps previously?
- [09:50]
B
Yes, we and others have noted that the age at diagnosis seems to have gone up. So, for example, when I was in training, the standard dictum was at the median age or the average age that people would get diagnosed would be about 30. And there are multiple different studies, including our Disco Ms. Study, where actually the average age at diagnosis was about 41. That age has sort of moved up over time. And we've also begun to have the discussion about late onset Ms. Late onset Ms. Is by definition with first symptoms after age 50. That accounts for about 8% or so of people. And then there's very late onset Ms. Over age 60, and that accounts for not quite 1% of people. So this concept that people are all 30 years old when they get diagnosed is not true. And that number has moved up over time, for sure. And we see it, and we saw it in the Disco Day, and we've seen it in other recent studies as well.
- [10:45]
A
Well, Dr. John Corboy, I want to thank you for all you do to improve the lives of everyone living with Ms. And thanks so much for talking with me.
- [10:52]
B
Thanks for having me, John. It's always a pleasure to see you.
- [10:54]
A
Myelin repair or remyelination is another research topic that you've told me is important to you. And while I was at the 2025 Actrooms forum, I also had an opportunity to speak with the 2025 recipient of the Barancik Prize for Innovation in Multiple Sclerosis Research, Dr. Mikhail Siemens. Dr. Siemens Foundational research on myelin biology really laid the groundwork for the research on myelin repair that's taking place today in laboratories around the world. Dr. Siemens was the first person to illustrate the actual biological processes responsible for creating, shaping and maintaining the myelin sheath. As a quick refresher, the myelin sheath is the fatty substance that surrounds nerve cells in the central nervous system. In ms, inflammation damages the myelin sheath, interrupting the ability of these nerve cells to communicate, leading to the broad range of symptoms and disabilities that are experienced by people living with Ms. Myelin repair is a natural process that eventually stops for people living with Ms. Dr. Siemens research has shed light on why that myelin repair stops, and understanding that process is fundamental to developing ways to restart it. In a moment, we'll hear my conversation with Dr. Mikhail Siemens. Doctor Mika Simmons is a neurologist and researcher at Technical University Munich and the center for Neurodegenerative Diseases in munich, Germany. And Dr. Simmons is this year's recipient of the Barancik Prize for Innovation in Ms. Research. Congratulations. Welcome to actroms, where you'll be delivering the Barancik Prize lecture. And welcome to Real Talk Ms.
- [12:45]
C
Thank you.
- [12:47]
A
What first interested you in multiple sclerosis research?
- [12:51]
C
So I studied medicine and did my residency in neurology. I started doing Alzheimer's research when I was a medical student. But I realized that the scope was a bit narrow at that time at least, and therefore I shifted, wanted to do something different. There are two reasons why I shifted to multiple sclerosis research. The first one is a clinical one. I like to work with patients with Ms. The second one is that I thought the biology of the disease is interesting for a scientist. It's an interdisciplinary problem that requires immunologists, neuroscientists, people that have expertise in glial biology. So I thought this is exciting to work on.
- [13:37]
A
Multiple sclerosis is a demyelinating disease. And your early research really laid the foundation for what many scientists continue to learn about myelin. Your subsequent research has revealed new information about the process of myelin repair. Can you tell me about your research on the effect of chronic inflammation on myelin repair?
- [13:58]
C
Certainly. To understand how myelin repair works, it's important to look at the immune system. So we think that one, that after a demyelinate event has happened, there is an inflammatory response that happens in the brain. We call this a reparative inflammation because it takes care of this damage. And so the cells, microglia, myeloid cells that are in the brain, they need to sense the damage, they have to take care of this damage and then they have to send factors to oligodendrocyte precursor cells to myelinate. So it's a very complex multicellular problem that we have. There are things that can be insufficient and go wrong. We have discovered a few of those pathways that we now try to target.
- [14:46]
A
Why does myelin repair fail sometimes? And what has your research uncovered about how the process can be restarted?
- [14:54]
C
So why does myelin repair fail? There are many reasons for this. We believe that one important reason is how the immune system functions and how it changes. And I refer to this reparative inflammation, this complex process of how the innate immune system instructs the precursor cells to myelinate. This is a delicate process and we have discovered cholesterol, metabolism and other pathways that can be insufficient. And this is one reason why myelin fails. There are also other problems that other people have found, like accumulation of myelin debris and inhibitory factors within deletions that contribute.
- [15:38]
A
But some of your research indicates the process can actually be restarted.
- [15:43]
C
That's true. So when we have a chronic inflammation in the brain, it's a kind of inflammation that sustains itself. It doesn't resolve. So that's what happens when this disease progresses. And there are certain factors that keep this chronic inflammation. One I refer to is lipid metabolism. Another one are CD8 tissue resident memory cells. These are long lived cells that lymphocytes that settle brain and remain there for a long time. And then there are interferon pathways. We need to dissolve and break this inflammation. If this would be successful, then we would reduce the damage and improve the repair.
- [16:24]
A
This could be a real game changer in Ms.
- [16:27]
C
If possible. So many people are working on this problem at the moment to target chronic inflammatory processes. The key is to come from experimental work in mouse, for example, and then validate this in humans to see if the principles are similar. There's one pathway that we have identified, this is related to interferon. This is also interferon gamma pathways. There are small molecules with which you could principle target this chronic inflammation. This needs to now be translated into trials, but we look forward to this.
- [17:00]
A
As you look at the Ms. Research that's taking place today, what excites you the most?
- [17:06]
C
I think the most exciting development at the moment are that we are starting to be able to target the progressive phase. So before, pharmaceutical industry and also researchers were focused on the first part of the disease. And a lot of progress have been made there. But the progressive pathology remains. We only partially understand it. But now there are first trials that have little effects on the relapses, but they have an effect on the progressive phase. They are still modest, this effect of the PTK inhibitors, but they might help us to understand the pathology of the progression better and we know what they actually do in the brain. And then it should be possible to find even better drugs that target this phase. Even better. This is one important aspect and another one I would like to add is on the cause and the origin of multiple sclerosis, where we know that environment plays an important role. But there's something missing in environment that is not yet understood. And I think research in this direction is very important. There has been interest on the Epstein Barr virus that plays a role from the environment, but possibly there are other viruses or other factors that we don't know. I think there is something big missing in the environment that needs to be discovered. If we know what it is, we could possibly design preventive therapies.
- [18:32]
A
I don't want to lose sight of the fact that you're here at the Outros Forum to receive the Barancik Prize. What does winning the Barancik Prize this year mean to you?
- [18:40]
C
So I'm very honored and grateful to win this award. It provides for me motivation to continue with my research. And this prize has. The foundation is valuing this translational research from bench to bench to bedside. And it provides me motivation to go along this path in my further research, to take the research from the lab and to the benefit of the patients at the end.
- [19:06]
A
And to that end, I want to thank you for all you do that ultimately impacts the lives of those patients at the end of the road there. Thank you so much for, for all the work you do and thanks so much for talking with me today.
- [19:17]
C
Thank you for having Me. Thank you.
- [19:20]
A
Fatigue is one of the most common Ms. Symptoms, affecting up to 80% of the people living with Ms. And I always describe fatigue as one of those symptoms that just gets in the way of life. It keeps you from fully engaging with your family or friends, and it's the number one reason people with Ms. End up up leaving the workforce. Last June, while I was at the Consortium of Multiple Sclerosis Center's annual meeting, I talked about fatigue with one of the leading Ms. Rehabilitation experts in the world, Dr. John DeLuca. In a moment, we'll hear that conversation. Doctor John DeLuca is a senior vice president for research and training and co director of the center for Multiple Sclerosis Research at Kessler foundation, as well as a professor in the physical medicine and rehabilitation and neurology departments at Rutgers New Jersey Medical School. And Dr. DeLuca's presentation at this year's CMSE annual meeting is entitled what does the Brain Tell Us about Fatigue? And I'll be asking you that in a moment, but first I'm hoping you'll explain how Ms. Related fatigue is measured.
- [20:34]
D
You know, it's really an important question because we've, for over 100 years we've been asking that question and we don't have a good answer. We do not have a good answer of how we measure fatigue. And so we don't have a good way of defining what it is. Therefore, we can't measure it, therefore how do we treat it? So it's a real problem. What we typically do is we use these instruments that presumably measure fatigue, but they're also contaminated by so many other factors such as sleep and deconditioning and such, that we really don't know what we're measuring. So it's a real problem, unfortunately.
- [21:12]
A
Why has fatigue proven to be so hard to treat? And I think you may have provided some of the answer just now.
- [21:19]
D
Yeah, it's been really hard because again, we have a hard time defining it and therefore we can't measure it. 19:21 Mucio asked, How do we define measure? An undefined entity. And we're still there today, and it's really a problem. So there may be things that we can do, but they're contaminated by other factors. If you use these instruments, therefore we're not really measuring it. Even if people feel better, the instruments don't tell us that they are.
- [21:46]
A
So now I'll go ahead and ask the question, what does the brain tell us about fatigue?
- [21:51]
D
You know, it's really interesting. So we look at what's called state Fatigue, that is fatigue in the moment, how do you feel right now? On a scale of 0 to 100, as opposed to trait fatigue, are these instruments that are contaminated by these questions? We put people in the MRI scanner and we cognitively fatigue them, and we measure their state fatigue before and after each one. And what we find is that state fatigue correlates with changes in the brain, functional changes in the brain, and that state fatigue does not correlate with trait fatigue, which does not correlate with changes in the brain. So what we know is that we have this brain network, and the hub of this brain network is the basal ganglia. And what's interesting is the basal ganglia is also the hub for the reward network in the brain. And so our approach is, if you can reward people, does reward actually reduce fatigue? And the data on that is actually yes. So the brain is telling us that if we understand how this network in the brain works, we understand this hub of the basal ganglia and its relationship between fatigue and on the other side, let's say reward, we can actually get to understanding how to measure it and then how to treat it.
- [23:08]
A
And it sounds like the nature of that treatment is non pharmacological.
- [23:13]
D
Well, that's actually, I think what happens right now. The best treatment for fatigue at this point is cognitive behavioral therapy. Okay. I think that ultimately there will be pharmacological. Pharmacological treatment, but it's gotta be more specific than what it is today. We have to understand the relationship between pharmacological therapy and reward, as well as just fatigue. And so I think we're gonna really move forward to understanding that relationship in that the brain is telling us what we need to look at.
- [23:43]
A
There's also been some evidence that exercise can mitigate several Ms. Symptoms, and fatigue has been listed as one of them.
- [23:51]
D
Yes, actually, there is. There is data on fatigue. And interestingly, when you think about the data that I know from our center, the other hub in the. In the fatigue network is the thalamus. And what's happening is that improvements from exercise are at the level of the thalamus. So that thalamus is also part of the fatigue network. So it all fits into a nice story. We just need to understand that relationship better. But if exercise is not rewarded, people won't do it.
- [24:23]
A
Exactly. Right. Anyone who has taken out a gym membership understands that principle, don't they?
- [24:28]
D
Exactly. So what we try to do is you try to ask patients what is rewarding for you that you haven't been able to do for a Long time. So let's say you haven't. I love to read, but I don't read anymore because I can't remember it. Well. We get them to join a book club or we get them to do something that's rewarding to them. And some people it's exercise. Some people it's something else. And that seems to be something that really helps.
- [24:53]
A
There are more than a few people dealing with Ms. Related fatigue who are listening to this conversation. Speaking generally, what's the best plan for mitigating that fatigue for someone with Ms. To pursue right now?
- [25:06]
D
Yeah, I think it's to be honest with yourself and say, what is it that I can do that I haven't been able to do, do, or I haven't wanted to do anymore? Be honest. You know, go out and try something that you'd love to do and stick with it. Start slow. Start slow. Be used to exercise. Start gardening. You know, start slow and try to build it up. Be honest with yourself and work with a professional, a neurologist, psychologist, occupational therapist to work on it. It's not going to happen overnight, but the brain is telling us that looking at what's happy, what makes us happy, what makes us really be motivated, can actually reduce fatigue.
- [25:50]
A
And that is perhaps the single best prescription I have ever heard.
- [25:55]
D
Well, thank you. And I think it can help even those of us who don't have Ms. For sure.
- [26:00]
A
Dr. John DeLuca, I want to thank you for all you have done and continue to do to really improve the lives of people who are living with Ms. And thanks so much for talking with me today.
- [26:09]
D
Oh, you. Thank. Thank you. It's been my pleasure, really.
- [26:12]
A
Over the past year, I've received a lot of questions about Ms. Progression, specifically the concept of progression independent of relapse activity. When we think about how Ms. Is categorized and described today, can someone really say that they've been diagnosed with relapsing, remitting Ms. And also say that they're experiencing progression independent of relapse activity? Sounds confusing, right? Well, while I was at the Consortium of Ms. Center's annual meeting, I listened to a panel discussion that addressed this confusion head on. The panel of Ms. Experts was facilitated by Dr. Steven Krieger. Dr. Krieger is a neurologist at the Corrine Goldsmith Dickinson center for multiple sclerosis at Mount Sinai in New York. And in my opinion, Dr. Krieger is redefining the standard of care when it comes to treating people living with Ms. The day after I listened to that remarkable and provocative panel Discussion. I had an opportunity to talk about it with Dr. Krieger. In a moment, we'll hear that conversation. Doctor Steven Krieger is a professor of neurology at the Icahn School of Medicine at Mount Sinai and a neurologist at the Corrine Goldsmith Dickinson center for multiple sclerosis. And Dr. Krieger led what I consider to be the most interesting and most provocative panel presentation at this year's CMSC meeting. It was entitled if Ms. Is One Disease, what Does that Mean for Clinical Conversations? Now, if you're a regular listener, you might recall that over the past year we've talked about whether the current Ms. Subtypes relapsing, remitting, secondary progressive, primary progressive, whether they're still relevant. Do they really do an adequate job of explaining or describing something specific about Ms. To patients and their doctors? So I thought this presentation was particularly well timed. Welcome back to the podcast, Dr. Krieger.
- [28:20]
E
John, thanks so much for having me. It's always a pleasure.
- [28:23]
A
How often do you find that a patient's experience doesn't neatly fit into one of the current categories that are used to classify ms?
- [28:32]
E
Well, as we've talked about before, I'm someone who feels that people in general are not categories and that categories are a way of organizing things, but rarely do justice to an individual person's experience, especially with something as diverse and personal as multiple sclerosis. And, you know, specifically, I've studied that even the way doctors write down what the diagnosis is in the chart can have a lot of uncertainty to it. And that between what we call relapsing, remitting, and what we call secondary progressive is a period of transition and uncertainty that can go on for years in the neurologist's mind and is probably going on forever in the life of the person.
- [29:22]
A
I sometimes wonder if anyone, if any patient has ever actually been told, I see you've just gotten secondary progressive Ms. Typically, that's something that you only get to really diagnose in the rearview mirror.
- [29:36]
E
I mean, you're absolutely right. It's diagnosed retrospectively because the way that category, that phenotype category was defined is a history of progression that has gone on for six months or more, and often much more. So one can never have a precise moment of transition from one category to another. And then I'd go one step further, maybe a little more provocatively, to say, if there's no moment that someone transitions from one category to another, are there really categories at all?
- [30:12]
A
Well, we've already started answering my next Question. In thinking about the presentation that you emceed with a phenomenal panel of experts, by the way, in addition to yourself, let's start with why is considering whether Ms. Is one disease, why is that important?
- [30:30]
E
Well, you know, one of the questions that kick started the creation of this panel and I'm really glad you found it provocative, I wanted it to be because I think that, you know, part of teaching is provoking people to think about things a little bit differently or asking hard questions. So the hard question that's kick started the development of that symposium was one that one of my patients asked me. He's a 30 year old man, I'd taken care of him for half a dozen years for Ms. He's on a high efficacy therapy, he's had no relapses, he's had no lesions, he has no findings, he's a lawyer, he has two young kids. And at the end of a visit, of course it's right at the end of the visit, your hands on the doorknob as the doctor might say. And he said, my wife wanted me to ask you, is it inevitable that I will transition to secondary progressive ms? And it's such a hard question to answer and it's such a heavy question that's not a light question. And you know, of course we're talking kind of philosophically about are there really categories? Right. But in, in the mind of someone who has a disease, a diagnosis, looks at information on the web, looks at the National Ms. Society of Information, there's these three types and that's what they mean. Of course someone's going to want to know that. And the fact that I can't answer that question or certainly the fact that it's an uncomfortable conversation I think speaks to the fact that we need to start thinking outside of those boxes a little bit. And I'll tell you, we discussed it with the panel and it was a great group of people. We had Dr. Cary Hirsch from Cleveland Clinic in Las Vegas, Dr. Juan oh from the Barlow Ms. Center in Toronto, Dr. Scott Newsome from, from Johns Hopkins, and Dr. Augusto Miravalle from Rush in Chicago. This is good that I just remembered all of that off the top of my head. But all of them had different takes on it and different takes on how to approach that question. But the one theme that came up is to say to that person asking that or to any one of your listeners wondering that kind of question, what are we really asking? And I think what was really being asked there was am I going to develop significant life changing Disability, is that going to happen? And, you know, the short answer is we don't always know. We have factors. We have good prognostic factors. We have great medicines in many ways. We don't always know. And I think it's really important for neurologists and Ms. Specialists to be able to administer our own uncertainty even while we do all the things that we're doing to try to make the outcome as favorable as possible.
- [33:19]
A
So given that if Ms. Is viewed as one disease, how might that impact patient care?
- [33:27]
E
Yeah, the idea is MS.1 disease. And I'll say there was not full consensus on this. I think at the end of the program here, we polled the audience which was, I don't know, about 100 people maybe, and 77% said, yes, Ms. is one disease. And the other 30 or so percent was less sure or wanted to stick with the categories.
- [33:47]
A
Well, they were the ones who were on their phones during the presentation, I think.
- [33:51]
E
Well, you know, listen, you can't reach all the people all the time, but you can reach some people. But, you know, if Ms. Is one disease. Well, for people who've been told they have relapsing, remitting ms, no evidence of progression can be a little bit unsettling. What does that mean? I no longer have relapsing, remitting Ms. You know, it's because it's been a comforting category. But we know that there's evidence of progression that can be subtle and can be biological that we can't always pick up. For people with secondary progressive Ms. Being told, well, now that's not a category anymore. That's not a thing. There's only one Ms. Well, maybe there's a little bit of optimism baked into that because I think the category SPMS has always been very foreboding. It presupposes that things are only going to get worse. And we know that that doesn't always happen. So I want it to be more honest. I don't want it to make people uncomfortable to say, what do I have now? I think it gives us an opportunity to say, let's not think in these boxes, let's pay more attention to you and not categorize and not say you have relapsing, remitting Ms. Therefore nothing's wrong, wrong, things might be wrong, and we need to pay attention to that and not to say to someone with secondary progressive ms, well, you're destined to get worse, because they might not be. And there's a lot of more empowering things people can do to stay stable and stay well, and keep their brain healthy. And I think we need to be open to that.
- [35:20]
A
Well, I can see where. When we're thinking about how it might impact the clinical conversation, I can see where it's going to end. Those conversations that leave the patient really confused because they'll hear, you know what? There's nothing new on your MRI scan, therefore, your Ms. Is stable. And they know since the last time they saw their treating physician, they're not doing as well, something's a little bit worse than it's been before. So they walk out of that office thinking, I didn't get my concerns really ever addressed in the conversation. And the expert who is in charge of my treatment plan just told me I'm stable, but I don't feel as stable as I did before. Maybe he or she doesn't really understand either.
- [36:11]
E
I mean, I think those are real conversations. I mean, your podcast is real Talk ms, and that's the real thing. That's the real conversation that happens. And I'll be honest, I struggle with that. It, as someone who takes care of people, sometimes I really can't find anything, any evidence that anything is worse. And in some ways that's good news, but it doesn't always do justice to what the person is feeling. And then I think the mandate needs to be to listen more carefully and to look harder and to take it seriously. You and I talked a year ago about looking below the surface and that the edss, or disability Scale, that all the trials, clinical trials use is imperfect, that the idea of somebody having an EDSS of 0 being perfectly normal is not true. It just means we hadn't looked carefully enough. And I think this conversation is in many ways an extension of that. It's saying the mandate for us as physicians, clinicians, people who treat patients with Ms. Is to center around the patient's story and their experience and not the labels that we have put on it for a long time.
- [37:29]
A
I could not agree with that more than I do. I think you already know. And you know, it occurs to me that the difference here. Well, several. But one of the big differences is that clinical conversation really becomes an evolving, ongoing dialogue that occurs and gets updated, as opposed to kind of a set of we check the box. As you pointed out, there's no signs of progression, and therefore you're not progressing, and someone walks away very confused. I think instead, this becomes a real conversation and we. And to me, what it sounds like is it opens the door to more personalized care where that patient who's in front of you Their issues are the ones that are going to be addressed.
- [38:22]
E
Oh, as you said it, you said it exactly right. It's personalized care categories are not people. And so getting away from categories and thinking about people and their individual experience with a disease I think is necessary to personalize the care. It came up in the symposium that we led. You know, Dr. Newsom talked about how we can assess patients in a more personalized and detailed way with wearable technologies. Other ways of monitoring folks to get outside of just a quick exam in the office. You look fine. That's not good enough, you know. So he looked at that. Dr. Oh Jiwon O talked about several things, but MRI in particular, that just because the MRI scan is stable, well, the MRIs that we have are not perfect. New technologies and new sequences on the MRI scan are going to show us things on the MRI that we didn't see before. So it allows us to look in more detail there. And perhaps the most kind of personalized aspect of it came from Dr. Hirsch and Dr. Miravalle who talked about about how can we harness well being and tools and techniques and strategies to foster brain health and body health and mental health. All of those are personalized because there's obviously no one size fits all way of making everyone's brain as healthy as it can be.
- [39:49]
A
Well, as I said a couple of minutes ago, I found this presentation to be the most compelling of them all. Having said that, switching gears for a minute. When you look at the Ms. Research landscape, what excites you?
- [40:04]
E
That's a tough question. Well, so yesterday at CMSC I was one of the presenters in the sort of clinical trials Science Update. And it was a whole series of presentations and what I thought was really remarkable, mine was the last one of the day. I talked about the phase two trial data for a medicine called Fraxalumab which Sanofi is developing. And it has done very well in the two years after its phase two trial and is now in phase three trials. And it has a totally novel way of working which I won't get into here, but it has just a mechanism that has never been used in Ms. Before. Before my talk there was a talk on fenibrutin, which is a medicine that Genentech is developing. They also supported the symposium that we were talking about. Fenibrutinib is a BTK inhibitor that's being looked at in progressive and relapsing Ms. And this was two year extension data from their phase two and that was successful. There was a Talk on a Car T therapy by Dr. Claire Riley from Columbia University in New York. She talked about preliminary data on how this entirely novel cell based mechanism could take out B cells in a way we've never so right there in this one session were three or four entirely new mechanisms that we don't have available to us in practice right now that are all on the cusp. And as we talk about personalizing treatment, it'd be nice to have medicines that work in a whole new set of ways to treat people in a whole new set of capacities.
- [41:44]
A
Well, I want to thank you for all the ways you treat people today who are living with ms, all the ways you pioneer future treatments as well. Well, thanks so much for talking with me. It is always my honor and pleasure.
- [41:56]
E
Listen, it's my honor and pleasure too. And as the field keeps moving, I hope we can keep doing this again.
- [42:02]
A
Count on it. That's going to wrap up this episode of Real Talk Ms. Real Talk Ms. Is powered by the National Ms. Society and you can share this episode of the podcast by letting your friends or family members know that all they have to do is point their web browser browser@realtalkms.com 433. You'll find that link in today's show notes so you can easily copy and paste it right into an email or a text. I hope you'll join me next week when we look back at the episode of Real Talk Ms. That you made the most popular in 2025. I'm John Strum. Thanks for listening. Stay safe and make make healthy choices. It.