Lessons for Parkinson’s From MS, and Vice Versa

This transcript has been edited for clarity. 

Indu Subramanian, MD: Hi, everyone. Welcome to Medscape. I’m so excited to have my friend and colleague, Prof Lorraine Kalia, join us today to talk about a very cool topic: what we can learn from multiple sclerosis (MS) studies and therapies, and how we can maybe translate that to some of the problems that we’ve been having in the Parkinson’s world.

Prof Lorraine Kalia is a clinical scientist at the Krembil Institute. She’s also an amazing neurologist at the University of Toronto, which is my alma mater. Welcome, Lorraine. 

Lorraine V. Kalia, MD, PhD: Hi, Indu. Thanks for having me. 

Meeting of MS and PD Minds

Subramanian: My name is Dr Indu Subramanian. I’m based at UCLA. Maybe we can get right into this. You had this very cool meeting in November 2022, and you had experts in the MS world as well as the Parkinson’s disease world. Tell us a little bit about what inspired that meeting in the first place. 

Kalia: It’s a bit of a personal story, actually. I might date myself a little bit, but I was a medical student during the time of the natalizumab development. At that time, I thought I was going to be an MS neurologist. 

Even back then, they already had a couple of disease-modifying therapies for MS and I thought, You know what, I think MS is good. I think they’re in good shape.

As a scientist with an understanding of the biology behind disease, it was clear to me that there still was a large amount of work needing to be done in Parkinson’s disease because that’s obviously how we translate things into having disease-modifying therapies. That was part of the reason — not the only reason — why I shifted into the movement disorder space.

Fast-forward many years later: I often give talks around the lack of disease-modifying therapies for Parkinson’s disease by introducing MS. Sometimes when you ask why we don’t have a disease-modifying therapy for Parkinson’s, people throw up their hands and say, “Well, you know, neurologic diseases are complicated.” 

I’ll often use the MS example to demonstrate that actually there is much that can be done in the neurologic space and there’s been a lot of successes in MS. 

I was once giving this talk, and as a consequence of this talk, had a conversation with Parkinson Canada who thought, wow, that’s an interesting idea around MS being so successful and PD lagging behind. We came up with the idea of having a meeting in Toronto. We obviously have very strong Parkinson’s researchers in Toronto, but also a very strong MS team at the Saint Michael’s Hospital. 

I collaborated with a colleague — actually, we were residents together — to bring world experts to Toronto to sit around a table, which is what we did, and talk about where we are in MS and where we are in Parkinson’s disease. We were looking for common ground but also looking to see what is different and how we might think about things differently that might have led to the different paths that we’ve experienced in our fields.

Lessons From MS

Subramanian: What do you think some take-home messages for the clinician would be from that discussion? I think it was a very cool paper.

Kalia: Maybe the take-home messages is it’s complicated, which is not as simple as I had hoped. I hoped that we’d come back with clear messages of what we really need to do with Parkinson’s. 

I think we found common ground for one thing. I think it’s fair to say that MS has done remarkably well at treating inflammation. All of their drugs are based on that, and they will recognize that they have challenges in terms of treating the neurodegenerative part of their condition.

Now that we increasingly recognize that inflammation is a part of Parkinson’s disease and there’s increased work around the immune basis to the disease, I think we are going to be able to take advantage of what MS has done and learn to hopefully make advances that way. 

For anybody who’s learned about MS , its successes have hanged heavily on its neuroimaging biomarkers of MRI. Of course, biomarkers are needed for the development of Parkinson’s disease , and perhaps more work into the neuroimaging piece as well as the biospecimen biomarkers is key to starting to be able to have different kinds of outcome measures. Not the clinical outcome measures that we’re using right now in basically all of our clinical trials, but to have early biomarker outcome measures that will help to inform us for our later clinical trials.

The other commonality between the two is this concept of earlier disease. We have our prodromal Parkinson’s disease and MS has their radiologically isolated syndrome. Up until now, logically, it has made sense to us that we should treat earlier in Parkinson’s disease, and that will likely give us better successes. In the MS space, there’s actually proof of that. They have clinical trials showing the benefit of treating people in the radiologically isolated syndrome state. 

While in Parkinson’s disease, it has been theoretical and seems to make sense to all of us, we don’t have any hard proof to say that treating earlier is better, whereas in MS they have already demonstrated that. I think this then provides us with actual proof in the pudding that that approach really does have implications for disease progression.

PD Ahead of MS for Lifestyle

Subramanian: Absolutely. I think both diseases in many ways have revolutionized since back in the day when we were in training. The MS models have really come a long way, with many patients doing very well for a long time. I think we have to really take a look at where our feelings are and how we can do better.

I’m excited just about the concept of identifying people early and then getting people who may be even at risk for developing Parkinson’s into lifestyle measures and wellness choices. I think MS has done a great job of that as well. Can you speak a little bit about that from your own perspective?

Kalia: I don’t think it came out in the paper, but it came out in our discussions that as a field and as a patient population, there’s probably been more embrace of lifestyle measures and physical activity in Parkinson’s, which I think is kudos to us in Parkinson’s disease. 

Maybe it’s in part because in MS they have these drugs that came through one after another after another, and there’s this heavy pharma management of MS that they haven’t had to explore the lifestyle assets.

There’s a large amount that MS has to learn from Parkinson’s disease, in terms of putting in place so many of the things that we discuss in Parkinson’s, whether it be diet, sleep, stress or mindfulness — all of these things. I think that in Parkinson’s, we’re further ahead.

Subramanian: Absolutely. I agree with you. I’m excited to learn from these other disease states that we train under in residency. We see these patients and we can open our minds to looking at different lenses, for sure. 

Thank you so much for spending the time and chatting about this. Kudos to you for having that meeting. It sounds like a great opportunity to bring great minds together.

Kalia: Yes. Hopefully, we can do more of this in the future.

Subramanian: Go Canada. Thank you for joining us, everyone. 

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