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Our Commitment to Reshaping the Future of Multiple Sclerosis

A microscopic illustration showing five purple neuron structures with glowing connections. There are two spheres set around them in different shades of purple. ​
Targeting neuroinflammation to try to halt MS progression

Multiple sclerosis (MS) is as unpredictable as it is complex. No two people experience the disease in the same way, and even when it seems like it’s under control, it might not be. Many people living with MS, especially a type called progressive MS, continue to experience disability progression even in the absence of relapses.1,2   

For a long time, we didn’t understand why this happened. Research focused on the sudden, acute “strikes” that caused the disease to get worse, and no one was looking at the underlying immune system processes working in the background.  

So we started looking.   

Understanding MS Differently

We expect to find immune cells acting erratically when they shouldn’t in diseases directly linked to immune processes, like autoimmune diseases or conditions that are driven by inflammation (like asthma, for instance).  

But many of these immune cells are also often found in diseases of the central nervous system (CNS), and we’re starting to understand how – instead of protecting us – they are doing long-term damage. This phenomenon is called neuroinflammation, and it’s contributing to diseases like MS.3  

How Neuroinflammation Works

Our central nervous system is protected by what’s called the blood-brain barrier – a border of cells that keeps substances in the blood stream from entering the brain. Sometimes this starts to break down, and when it is damaged, immune cells that aren’t supposed to be there can cross the barrier and start to cause trouble.3  

These cells may start to attack healthy neurons (brain and spinal cord cells), causing damage. It happens quickly, like a sudden strike, and brain cells do have ways to fight back. But the rogue immune cells have another secret force – they “recruit” specific brain-protective immune cells to help them. Those cells, called microglia, live inside the blood-brain barrier and are solely intended to protect the CNS.1,2,4,5  

But when immune cells attack, they can erroneously set these microglia against healthy cells, too. So even after damage may be repaired, these microglia, trapped inside the CNS, are still activated against the neurons and can cause slow but progressive damage – what is called smoldering neuroinflammation.1  

Different parts of the brain are then influenced by this damage, and neuroinflammation continues to compound the damage over a long time. The cells degenerate and start to malfunction.1,2  

Our goal is simple: to help people with MS live for the moment, and not the disease.

How We’re Working to Advance Science to Help Improve Lives

MS is characterized by this neurodegeneration – when cells in the brain and other parts of the nervous system lose function and eventually die. It causes a decline in nerve control and physical function, and eventually mobility.6   

But for a long time, researchers didn’t realize how neuroinflammation might be contributing to neurodegeneration. We thought completely differently about neurological diseases involving the CNS and inflammatory conditions involving the immune system.  

Now we know differently. It is more than sudden relapses that are driving the devastating and destructive progression of MS, but also the chronic, smoldering neuroinflammation.1 We’re blazing a transformative scientific path by uncovering the connections between our immune system and nerve cells with the goal of finding new ways to halt the disease and help people around the world who are living with MS.

This means leveraging our deep knowledge of immune processes to try to stop neuroinflammation in its tracks, slow disease progression and hopefully improve the quality of life for patients who need it most. Our goal is simple: to help people with MS live for the moment, and not the disease.  

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References

  1. Giovannoni G, Popescu V, Wuerfel J, et al. Smouldering multiple sclerosis: the ‘real MS’. Ther Adv Neurol Disord. doi:10.1177/17562864211066751
  2. Frisch ES, Pretzsch R, Weber MS. A Milestone in Multiple Sclerosis Therapy: Monoclonal Antibodies Against CD20—Yet Progress Continues. Neurotherapeutics. 2021;18:1602-1622. 
  3. Häusser-Kinzel S, Weber MS. The role of B cells and antibodies in multiple sclerosis, neuromyelitis optica, and related disorders. Front Immunol. 2019;10:201. 
  4. Scalfari A. MS can be considered a primary progressive disease in all cases, but some patients have superimposed relapses - Yes. Mult Scler.2021;27(7):1002-1004. 
  5. Matejuk A, Ransohoff RM. Crosstalk Between Astrocytes and Microglia: An Overview. Front Immunol. 2020 Jul 16;11:1416. doi: 10.3389/fimmu.2020.01416. PMID: 32765501; PMCID: PMC7378357. 
  6. Absinta M, Sati P, Masuzzo F, et al. Association of chronic active multiple sclerosis lesions with disability in vivo. JAMA Neurol. 2019;76(12):1474-1483. 

MAT-GLB-2505755 I October 2025