Hi, I'm Cristina Granziera. I'm part of a member of the Executive Committee of ECTRIMS. I'm also a neurologist, clinically active at the University Hospital Basel, and I'm co-directing the Research Center for Clinical Neuroimmunology and Neuroscience in Basel.
So ECTRIMS this year was a special ECTRIMS because it was the 40th anniversary of the conference. And in addition, for the first time, we had the so-called pre-day, which is a day that was focusing on pediatric MS, neuromyelitis optica spectrum disorders, and MOGAD, and also autoimmune encephalitis. So, the overall themes have been expanded this year with this pre-day. Nevertheless, we still had a strong focus on diagnostic, prognostic, and on progressive MS.
The first thing I would mention is the update of the diagnostic criteria, which was the result of a consensus meeting that we did some while ago. And these results were groundbreaking because for the first time, there was the intent to increase the specificity of these criteria through the introduction of novel biomarkers, especially imaging biomarkers such as the central vein sign and paramagnetic rim lesions.
In addition to that, there was the introduction of the fifth topography for MS diagnosis, which is the optic nerve. So really novel approaches to the way of thinking to improve specificity, which will definitely benefit the patients because we hope it will substantially reduce the number of misdiagnoses.
I'm David Hafler. I'm chairman of the Department of Neurology and professor of immunobiology at the Yale School of Medicine.
There was a presentation related to BTK inhibitors, it’s a very hot area, which seemed to have a potentially positive signal in patients with progressive MS, whereas it didn't seem to work very well in patients with earlier autoimmune form of MS, relapsing remitting form of disease. We've yet to really see the data, to see how strong they really are. I think that was probably an important part of it.
To me, another really interesting area was in the genetics of MS work presented by Steve Sawcer, where the International MS Genetics Consortium, of which I'm a member, was able to show that there are genetic variants associated with progression and those genetic variants were replicated looking into that autopsy sample, the patients with MS. That is, MS Genetics Consortium a number of years ago identified genetic variants associated with disease risk. And they were affecting predominantly immune genes, suggesting that early MS is in fact an autoimmune disease, whereas progressive disease seems to be very different. And this was really confirmed by the genetic analysis, which showed that the genetic variants associated with progression are predominantly in the brain and central nervous system.
I would argue that we have a pretty good idea what causes relapsing-remitting multiple sclerosis and the ability to stop it with B-cell depletion, which should probably always be a first-line drug. It's given us a great indication of the disease. The big unknown is what actually triggers the disease. How does it get started? And there's very strong evidence that the Epstein-Barr virus is a critical trigger in a genetically susceptible host. One of the big areas to me of interest is to understand how the EBV virus can actually trigger the immune system. Is it just cross-reactivity with brain antigens, which probably occurs, or does it activate the immune system in a genetically susceptible host? Because of course, EBV infects B cells. So, the ability of the B cells to so-called break tolerance and allow the immune system to become activated is critical. So, I think understanding of how EBV actually triggers MS is going to be an important breakthrough next year.
