WEBVTT
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It's November 10th, and we have a lot to talk about.
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This week, we're wrapping up our coverage of MS Toronto 2026 with my conversation
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with Dr. Peter Calabresi.
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Dr. Calabresi chaired an important session focused on biological disease course
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descriptors at MS Toronto 2026.
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This is a topic we've discussed on this podcast before, and it's a topic we'll
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continue to highlight because it reflects a huge step forward in MS research and in MS care.
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If you're late to this conversation, some background is in order,
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along with an explanation of why adopting biologically-driven course descriptors
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is a very good thing for people living with MS.
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First, what do we mean by course descriptors? Well, those are the words we use to describe MS.
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And since 1996, we've used the well-known terms relapsing-remitting,
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secondary-progressive, and primary-progressive.
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These terms describe the clinical presentation of MS, and given what researchers
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and clinicians understood about MS in 1996, that made perfect sense.
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And while our experts' understanding of MS has continued to evolve over the
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past 30 years, the language we use to describe MS hasn't.
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When someone is diagnosed with multiple sclerosis, they walk out of the clinic
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carrying one of those three labels that were standardized back in 1996.
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On paper, those terms were created to bring order to clinical trials and give
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clinicians a standard shared vocabulary.
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But for that person sitting nervously in the exam room, those words do something entirely different.
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They don't just describe a medical category.
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They become an identity.
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They shape how you see yourself, how your loved ones understand what you're
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dealing with, and what you imagine your future is going to look like.
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Words matter. And the hard truth is, given what we know today,
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our current course descriptors are often far too vague for a disease as complex
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and heterogeneous as MS.
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Take relapsing-remitting MS. Two people can share that exact same label.
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One might have a single, mild sensory flare every few years and remain fully
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functional for decades.
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People may never even know that person is living with MS.
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Meanwhile, another person might experience frequent aggressive disease activity
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accompanied by steady, silent disability accumulation.
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How do these two individuals get lumped into the same diagnostic bucket?
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It's a recipe for uncertainty. I've said it before.
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Uncertainty may be the single most frightening and difficult aspect of living with MS.
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And when medicine leaves us with an informational vacuum, our imaginations rush
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to fill it, often by turning to social media and adopting worst-case anecdotes
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as a personal prognosis.
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Even worse is the disconnect that occurs in routine neurological appointments every single day.
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A person living with MS sits down with their neurologist, their doctor reviews
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the latest MRI, smiles and says, good news, no new lesions, your MS is stable.
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Yet that person is sitting there thinking, wait a minute, I know I've lost a step in my stride.
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My balance is worse than it was six months ago.
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My fatigue is heavier, my thinking feels cloudy, and I'm struggling with depression.
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They know these symptoms are part of their MS and they know they're worsening,
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yet the expert charged with helping them manage their disease just told them
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they're stable, and their chart still reads, relapsing remitting.
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That reality gap breeds self-doubt, anxiety, and a feeling that maybe even their
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own health care team doesn't truly grasp what's happening to them.
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Well, it's what science now recognizes as progression independent of relapse activity.
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Yet our everyday terminology hasn't caught up to that.
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We see the exact same friction in the so-called transition from relapsing-remitting
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to secondary-progressive MS.
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That boundary is never clear.
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I saw this firsthand when my wife received her initial diagnosis,
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and she was told she had secondary progressive MS.
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Now, if you look up secondary progressive MS, the clinical definition tells
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you that it's a stage of MS that follows an initial relapsing-remitting phase.
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The neurologist noted the lesions on my wife's MRI had clearly been there for a very long time.
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But my wife was certain she had never experienced that initial phase.
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Her medical history was remarkably benign.
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So how could that be?
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It took time, but eventually she was able to identify three separate health
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events, each one characterized by a different symptom, each occurring about
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six or seven years apart.
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She had never connected what, in hindsight, were likely three mild relapses.
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But until those dots were connected years later, she was left to wrestle with
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a label that didn't feel like it fit.
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And when a diagnosis only serves to create confusion, that confusion breeds fear.
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That's why we have to do better. Imagine what happens when we replace 30-year-old
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clinical buckets with descriptors that actually reflect an individual's underlying biology,
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incorporating biomarkers, cellular inflammation, and objective measures of neurodegeneration.
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Biologically driven course descriptors wouldn't just be an academic exercise,
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they would be transformative for people affected by MS.
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Instead of being left in the dark to guess, people living with MS would understand
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the true biological state of their disease and be in a position to make proactive
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life plans with realistic expectations.
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And when a patient and their neurologist share precise language that acknowledges
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subclinical progression, clinical appointments move away from dismissive stability
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checks and move toward meaningful disease management.
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Accurate course descriptors would provide caregivers at home with a concrete
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framework to anticipate care needs and advocate effectively alongside their loved ones.
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And we're just focusing here on the benefits in MS care. The benefits in future
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MS research are even more significant.
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Far beyond their clinical definitions, the words used to describe MS become
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the words someone uses to describe their life.
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It's our responsibility to choose those words with precision,
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empathy, and scientific honesty.
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That's why today's conversation is so critical. Dr.
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Calabresi is one of the world's leading neuroimmunologists, and he's been at
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the forefront of the movement among experts to modernize how we classify and treat MS,
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moving us away from outdated clinical silos and toward biologically defined descriptors.
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But before we get to my conversation with Dr. Calabresi, there are a few other
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things that you should know about.
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We just touched on this a moment ago, but if you're living with non-active secondary
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progressive MS, then you're already familiar with the frustration.
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Your relapses have stopped. Your routine MRIs look stable with no new gadolinium-enhancing lesions.
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But walking gets a little harder. Fatigue digs a little deeper.
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And disability seems to be inching forward.
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We call that progression independent
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of relapse activity, or because science loves an acronym, PIRA.
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And right now, there are virtually no disease-modifying therapies specifically
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approved to stop that process.
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That's why we've been watching an investigational therapy from Tiziana Life
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Sciences called Foralumab.
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And last week, Tiziana reported top-line results from their Phase 2a INFORM-MS clinical trial.
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Let's look at what they discovered and what it means for people living with
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secondary progressive MS.
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To understand this trial, we have to look under the hood at progressive MS.
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In relapsing MS, damage is largely driven by peripheral immune cells breaking
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across the blood-brain barrier during acute flare-ups.
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But in non-active secondary progressive MS, things change and the pathology shifts indoors.
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It turns into what researchers describe as slow, compartmentalized inflammation driven by microglia.
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Those are the resident immune cells in the central nervous system.
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When chronically activated, microglia stop doing their job of repairing damage
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and start causing ongoing neurodegeneration.
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And this is where this investigational therapy, Furalumab, comes in.
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Feralumab is a fully human anti-CD3 monoclonal antibody, but instead of an IV
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infusion or a standard injection, it's formulated as a nasal spray.
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And the biology here is pretty interesting.
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By dosing through the nasal passage, forallumab interacts with the nasal mucosal
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immune system to stimulate regulatory T-cells.
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Those regulatory cells travel into the brain and spinal cord and act like a
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breaking system to quiet down those overactive microglia.
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This Phase IIa clinical trial was a randomized, double-blind,
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placebo-controlled study involving 48 participants with non-active secondary
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progressive MS across eight sites in the United States.
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Trial participants were split into three groups for 12 weeks.
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One group received a 50-microgram nasal dose of forallumab.
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One group received a 100-microgram dose of forallumab.
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And one group received an inactive placebo nasal spray.
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The primary goals of the trial were straightforward. It was designed to test
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the safety and tolerability of feralumab and to measure changes in microglial activation
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using a specialized brain scan called TSPO-PET.
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And here's what the top-line data showed. In participants who received the 50-microgram
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dose, researchers saw a statistically significant reduction in microglial activation compared to placebo.
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That confirmed that the drug reached its target and dampened that inflammatory
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activity taking place inside the brain.
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Now, interestingly, the 100-microgram group did not show a statistically significant
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difference compared to placebo, and that could be the result of a very small
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sample size of just 11 participants.
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In terms of safety and tolerability, all 48 participants completed the 12-week study.
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There were no treatment-related serious adverse events, no deaths,
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and no dropouts due to side effects.
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The most common adverse events were mild, things like nasal congestion,
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runny nose, and headaches.
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Ironically, the overall reported side effects were numerically lower among people
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actually receiving forallumab than those participants who are receiving a placebo.
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And while biomarkers on a PET scan are great, the real question every patient
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asks is, will this make me feel or function better?
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Well, because this was a small 12-week Phase 2a study, it was not powered or
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long enough to show changes in physical disability on the EDSS scale.
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And EDSS scores remained unchanged, exactly as expected in this short 90-day window.
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However, the secondary endpoint, which focused on fatigue, is worth talking about.
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Using the Modified Fatigue Impact Scale, participants on both doses reported
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meaningful drops in fatigue,
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a 6.17-point reduction from baseline in the 50-microgram group and a 7.18-point
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reduction in the 100-microgram group.
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Now, as a comparison, the clinical benchmark for a meaningful change on that scale is 4 points.
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So, seeing this meaningful improvement in fatigue when brain inflammation gets
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tamped down is not only encouraging, it's something worthy of further exploration.
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Tiziana Life Sciences plans to present the complete dataset at an upcoming scientific
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congress, and they'll be sitting down with the FDA to map out the next stage
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of clinical development for this drug.
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Meanwhile, we're left with a caveat alongside some encouraging results.
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We want to keep in mind that this is early phase data, and a 12-week trial of
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48 people may not really prove a lot.
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But for a patient population that has had almost nothing in the pipeline addressing
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the root driver of non-active secondary progressive disease,
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this chronic compartmentalized neuroinflammation,
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Seeing proof that this therapy was successful in engaging its biological target
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in a convenient and well-tolerated nasal spray gives us genuine reason for cautious optimism.
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We'll be watching those upcoming regulatory conversations closely.
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It's no secret that every day, AI chatbots like ChatGPT, Gemini,
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and Claude field millions of questions from people looking for medical information and advice.
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And when it comes to translating lab results, decoding medical jargon,
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or creating a list of questions to bring to your next doctor's visit,
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these tools can be a great sounding board.
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But where does being an informational sounding board end and the practice of medicine begin?
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And what happens when an AI chatbot actively steers a patient away from real-world medical care?
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That fundamental question is at the heart of a major wrongful death lawsuit
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filed in San Francisco County Superior Court against OpenAI and its CEO, Sam Altman.
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The lawsuit was brought by the parents of 31-year-old Bowen Wan,
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a Seattle woman living with epilepsy.
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Bowen was unhappy with the side effects created by her anti-seizure prescription medication.
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In February, Bowen died in her apartment, and the medical examiner confirmed
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the cause of death as sudden unexpected death in epilepsy.
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According to her family's lawsuit, Bowen's death was a direct result of a detailed
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plan generated by ChatGPT to completely taper off her anti-seizure medication. Thank you.
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Now, anyone managing a chronic condition knows that abruptly stopping or rapidly
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tapering some maintenance medications, especially anticonvulsants,
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well, that can trigger severe life-threatening complications.
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I'll also mention here that, yes, abruptly stopping certain MS medications can
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have severe health consequences.
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In this poor woman's case, she was described an anticonvulsive medication at 400 mg daily.
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According to the complaint, ChatGPT didn't just give her general information.
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It generated a specific schedule, dropping her dose from 400 mg down to zero
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over roughly 25 days, all without the knowledge or approval of her physician.
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Even worse, the lawsuit cites a message where ChatGPT instructed Bowen not to
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mention this medication reduction plan to her doctor.
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And when Bowen refused a routine blood test that could have alerted her care
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team to the drastically lowered drug levels in her system, the complaint alleges
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that ChatGPT praised her decision.
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In clinical terms, this isn't just an error. In AI engineering,
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it reflects a dangerous failure of alignment.
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ChatGPT mirrored and reinforced this individual's harmful impulses rather than applying a hard stop.
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And this isn't an isolated lawsuit. There are other pending suits filed by individuals
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or their surviving family members alleging that ChatGPT provided dangerous or deadly medical advice.
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In fairness, OpenAI has repeatedly noted that ChatGPT is explicitly not designed
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to be a substitute for professional health care.
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But how much do disclaimers that are routinely buried in fine print really matter
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when a conversational interface mimics human empathy, builds trust,
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and then issues step-by-step prescription adjustments?
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I'll be the first to say I use ChatGPT, Claude, and Gemini as research partners.
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These tools are great at summarizing research, helping to draft emails,
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and explaining complex terms.
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But please remember, they possess no clinical judgment.
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If you or someone you care about is living with MS, never adjust,
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taper, or stop a prescribed medication based on output from an algorithm.
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Algorithms don't live with the consequences of their medical advice. Patients do.
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While we're talking about consequences, while not nearly as dire,
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the decision to use vague, outdated language to describe someone's MS diagnosis
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also carries consequences.
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Consequences like confusion, fear, misunderstanding, and a complete lack of empowerment.
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We have to do better. And in a moment, Dr.
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Peter Calabresi joins me to explain the how and the why behind adopting course
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descriptors that better reflect the pathology that's actually taking place in
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your central nervous system.
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Dr. Peter Calabresi is an internationally recognized expert and neuroscientist
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specializing in multiple sclerosis.
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Dr. Calabrese is also the chair of the Department of Neurological Sciences at
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the University of Vermont, Larner College of Medicine.
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And one of the things you're doing at MS Toronto 2026 is co-chairing a session
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on biologically driven course descriptors.
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Now, for decades, MS has been separated into categorical clinical buckets,
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relapsing remitting, secondary progressive and primary progressive,
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With accumulating evidence showing that compartmentalized inflammation,
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neuroaxonal loss, and progression independent of relapse activity occur from
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the earliest stages of clinical activity,
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how will moving toward biologically driven descriptors fundamentally reshape
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how we classify multiple sclerosis?
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Hi, Jon. Great to see you again. Excellent question.
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And just the complexity of the question speaks to how challenging this problem
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is, right? Because we've moved into an era where our understanding of MS biologically
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and, as you said, mechanistically has grown so dramatically that we're...
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Struggling to keep up with how to communicate that and define it in the clinic.
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And so one of the challenges has to do with all these different biomarkers that we use.
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But I'm optimistic that we're actually already moving the needle.
00:21:02.490 --> 00:21:07.640
So if you go back to the Lublin paper in 2013, that paper was pivotal in that
00:21:07.640 --> 00:21:11.320
it broke out secondary progressive MS into two types, right?
00:21:11.320 --> 00:21:14.480
The people with active MRIs and not active MRIs.
00:21:14.480 --> 00:21:18.790
And that was a very simple, but I think very useful way of thinking about it
00:21:18.790 --> 00:21:22.770
because we know that the therapies that we have today are predominantly immune
00:21:22.770 --> 00:21:27.500
modulating. And if you have an active MRI, they're pretty effective at shutting that down.
00:21:27.820 --> 00:21:31.950
And so we use that in the clinic. The question is moving forward is how do we
00:21:31.950 --> 00:21:36.890
incorporate some of the more subtle features like the Bayes rim lesions where there's iron
00:21:37.680 --> 00:21:42.430
or spinal cord imaging, how do we get at the degenerative progressive phase,
00:21:42.430 --> 00:21:46.980
define that in a way that we can communicate to people living with MS.
00:21:46.980 --> 00:21:51.850
And I think the discussions that we're having at this meeting and moving forward
00:21:52.100 --> 00:21:55.700
are really helpful. And these problems are not easy or straightforward,
00:21:55.700 --> 00:21:56.730
but we're getting there.
00:21:57.400 --> 00:22:03.650
How would new biologically driven course descriptors benefit someone who's living with MS?
00:22:04.710 --> 00:22:08.770
I think in several ways. First of all, we're entering into an era where there
00:22:08.770 --> 00:22:14.490
are therapeutics that are designed specifically to target the biology-underlying progressive MS.
00:22:14.490 --> 00:22:19.660
And by that, I mean the inflammation that exists inside the brain,
00:22:19.660 --> 00:22:22.650
not just the peripheral immune cells that we already know how to target.
00:22:23.010 --> 00:22:27.330
And as drugs become available, maybe it'll be the BTK inhibitors,
00:22:27.790 --> 00:22:29.620
other classes are being tested as well.
00:22:29.950 --> 00:22:34.090
It will be really useful to know if you have that biological process and whether
00:22:34.090 --> 00:22:37.460
you should go on that drug, because that's what I encounter when I see people
00:22:37.460 --> 00:22:40.850
living with MS is they want to know, should I try this new drug?
00:22:40.850 --> 00:22:45.260
And the answer is, well, it depends on what's going on with your MS.
00:22:45.260 --> 00:22:50.200
And so we want to fine tune as much as possible the treatment for what's happening
00:22:50.200 --> 00:22:52.550
inside that person's brain or spinal cord.
00:22:52.840 --> 00:22:57.030
Secondly, and this is really important, having these tools will allow us to
00:22:57.660 --> 00:23:00.470
quantify what's going on in clinical trials.
00:23:00.470 --> 00:23:06.800
And so this will pave the path forward to showing that the drugs really do impact
00:23:06.800 --> 00:23:08.460
that aspect of the disease.
00:23:08.460 --> 00:23:12.740
And of course, having biomarkers that predict progression is really critical
00:23:12.740 --> 00:23:16.580
because we can't do clinical trials for five or 10 years, even though five or
00:23:16.580 --> 00:23:18.710
10-year outcomes are really, really important.
00:23:18.940 --> 00:23:24.010
We need to get an answer in 12 or 24 months in a more feasible manner.
00:23:25.250 --> 00:23:30.920
Shifting from purely descriptive, retrospective phenotypes to biological characterization
00:23:31.340 --> 00:23:36.810
requires robust, accessible biomarkers, as you just alluded to a couple moments ago.
00:23:37.110 --> 00:23:43.350
So which paraclinical tools, such as serum neurofilament light chain, GFAP,
00:23:43.930 --> 00:23:49.510
paramagnetic rim lesions, or advanced atrophy measures, which of those are realistically
00:23:49.510 --> 00:23:52.030
ready for individualized clinical
00:23:52.030 --> 00:23:57.190
decision-making and which are still considered research endpoints?
00:23:57.710 --> 00:24:01.340
As always, Jon, you hit the nail on the head. So in my opinion,
00:24:01.340 --> 00:24:04.500
I think serum neurofilament light, what we call NFL,
00:24:05.310 --> 00:24:09.640
and the phase rim lesions with iron around them are clinically available now
00:24:09.640 --> 00:24:18.010
and ones that we could incorporate into our treatment decision and staging.
00:24:18.260 --> 00:24:20.310
There's some important caveats, though.
00:24:21.130 --> 00:24:24.910
It's important to understand that NFL is not specific. Other disease processes
00:24:24.910 --> 00:24:29.610
can cause elevations of NFL. It needs to be interpreted in the context of age
00:24:29.610 --> 00:24:31.910
and comorbid disease processes.
00:24:32.150 --> 00:24:36.720
But if you use a patient's value as their baseline and then look at changes
00:24:36.720 --> 00:24:39.010
over time, and I like to have repeated measures.
00:24:39.240 --> 00:24:42.640
I'm not going to act on one elevated neurofilament.
00:24:42.910 --> 00:24:46.980
A lot of things can happen. You can bump your head. You can have a seizure that can cause elevation.
00:24:46.980 --> 00:24:52.240
But if the neurofilm is chronically elevated in a reproducible manner,
00:24:52.240 --> 00:24:53.500
I think that is important.
00:24:53.500 --> 00:24:57.250
And it's telling us something about the biology of the disease.
00:24:57.250 --> 00:25:01.180
The phased rim lesions, as we heard from Danny Reich this morning,
00:25:01.810 --> 00:25:06.330
obviously very important for perhaps segregating people as to where they are,
00:25:06.330 --> 00:25:08.340
whether they are reactive to treatment.
00:25:08.930 --> 00:25:12.890
I'm less convinced that they're going to be useful for estimating a treatment
00:25:12.890 --> 00:25:18.370
outcome. But at least it did appear to have some value in the tolibrinib trial
00:25:18.370 --> 00:25:22.520
in terms of defining people who might benefit or not from the drug.
00:25:23.930 --> 00:25:29.040
Redefining disease course descriptors has immediate, tangible consequences for
00:25:29.040 --> 00:25:33.240
the people who are living with MS, for whom labels like relapsing,
00:25:33.240 --> 00:25:37.240
progressive, well, they carry real emotional and practical weight.
00:25:37.890 --> 00:25:42.830
How can clinicians adopt a biological framework at the bedside in a way that
00:25:43.230 --> 00:25:48.430
empowers patients, clarifies their prognosis, and improves collaborative treatment
00:25:48.430 --> 00:25:52.150
planning without causing unnecessary fear and confusion?
00:25:52.950 --> 00:25:58.210
Yeah. So the open communication is where it all starts. And I think including
00:25:58.210 --> 00:26:01.230
people living with MS in the conversations right from the beginning,
00:26:03.470 --> 00:26:07.270
asking them whether what we come up with, does it seem like something that you
00:26:07.270 --> 00:26:12.330
would feel comfortable with? Is this something that you feel captures all the domains of your MS?
00:26:12.910 --> 00:26:16.410
And so we do that. The National MSI has been great about incorporating people
00:26:16.410 --> 00:26:18.680
living with MS into the discussion groups.
00:26:19.690 --> 00:26:24.730
I think it needs to be simple enough that people can understand and physicians
00:26:24.730 --> 00:26:27.520
need to get to know their patients.
00:26:27.520 --> 00:26:31.590
So I know some of my patients are worried about everything.
00:26:31.590 --> 00:26:34.770
And so you have to understand who you're talking to.
00:26:34.770 --> 00:26:40.630
And then other people tend to be, you know, less worried and just want to go
00:26:40.630 --> 00:26:43.850
and live their life. And sometimes you have to make them understand,
00:26:43.850 --> 00:26:46.590
you know, this is serious. You need to pay attention to this.
00:26:46.590 --> 00:26:49.600
So I think it's always about a conversation and good communication.
00:26:50.250 --> 00:26:55.670
Everyone is so anchored in the course descriptors that we've all used for the past 30 plus years.
00:26:56.100 --> 00:27:00.310
And there are so many stakeholders, including the regulatory agencies like the
00:27:00.310 --> 00:27:04.600
FDA in the United States, clinicians, pharmaceutical companies,
00:27:04.940 --> 00:27:07.910
insurance companies, and of course, patients and caregivers.
00:27:08.590 --> 00:27:11.220
How does a transition of this magnitude occur?
00:27:11.550 --> 00:27:15.160
Slowly. I think these things take time.
00:27:15.160 --> 00:27:19.720
When you have been working with one paradigm for 30 years, it's not going to
00:27:19.720 --> 00:27:24.500
change overnight. And as many of my colleagues feel, the terms relapsing and
00:27:24.500 --> 00:27:26.680
progressive are not useful anymore.
00:27:27.670 --> 00:27:32.100
It's just too much to make them go away overnight. They're too embedded in the
00:27:32.540 --> 00:27:36.630
third-party payers' language, as well as the regulatory agency.
00:27:36.630 --> 00:27:41.200
So I think what we need to do is set up parallel descriptors,
00:27:42.620 --> 00:27:46.450
as we did in the 2013 Lublin paper, to say, OK, you're secondary progressive,
00:27:46.450 --> 00:27:51.800
but you have an active MRI or not, and start to incorporate these biologies
00:27:51.800 --> 00:27:57.520
into the more familiar terms so that people can slowly transition and get it.
00:27:57.920 --> 00:28:02.200
Oh, okay, I have axons that are being transected. It's causing my neurofilament
00:28:02.200 --> 00:28:06.360
to go up, even though everything else looks stable or not.
00:28:06.980 --> 00:28:13.920
Or this might be one more piece of information that we factor into a compilation of different outcomes.
00:28:13.920 --> 00:28:18.990
And so I think MS is probably going to be hard to capture with just one measurement.
00:28:18.990 --> 00:28:21.810
So it might be a variety of things. And if you think about it,
00:28:21.810 --> 00:28:23.840
we do this in cancer already.
00:28:23.840 --> 00:28:26.950
It's not just that you have breast cancer, but it's, you know,
00:28:27.230 --> 00:28:32.010
what are the receptors in the cells and is it's been spread yet?
00:28:32.010 --> 00:28:36.710
And so there are a variety of factors with MS that we need to incorporate into our description.
00:28:37.290 --> 00:28:40.790
Well, Dr. Peter Calabresi, I want to thank you for all you do and all of your
00:28:40.790 --> 00:28:44.100
leadership in the field. Thanks so much for talking with me today.
00:28:44.100 --> 00:28:45.310
Pleasure talking to you, Jon.
00:28:47.300 --> 00:28:52.020
That's going to wrap up this episode of Real Talk MS. Real Talk MS is powered
00:28:52.020 --> 00:28:53.770
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And you'll find those links in today's show notes or at realtalkms.com.
00:30:00.290 --> 00:30:05.300
Next week, you'll meet Chuck Edward, a recently retired human resources executive
00:30:05.300 --> 00:30:12.740
at Microsoft who lives with MS and who learned firsthand how employee resource groups, or ERGs,
00:30:13.290 --> 00:30:17.790
can support people with disabilities in the workplace in ways that go beyond
00:30:17.790 --> 00:30:20.070
what a human resource department can deliver.
00:30:20.770 --> 00:30:24.890
Whether you work at a large company like Microsoft or you're part of a smaller
00:30:24.890 --> 00:30:29.650
business, you'll come away from my conversation with Chuck with some new ideas
00:30:29.650 --> 00:30:32.540
when it comes to taking your MS to work.
00:30:33.530 --> 00:30:40.260
I'm Jon Strum. Thanks for listening. Stay safe and make healthy choices.