One of the world’s leading research sites for multiple sclerosis, The Centre for Brain Research in Vienna, and one of its lead researchers, Dr. Hans Lassmann, Head of the Department of Neuroimmunology, point to inflammation and neurodegeneration as culprits in progressive multiple sclerosis (MS), according to research published this month in The Lancet. This new understanding of how the disease progresses could lead to new treatment modalities.
In the autoimmune disease of MS, the body’s own immune system attacks the myelin coating of nerve cells. This neurodegeneration results in neurological disability in those with MS. With relapsing/remitting MS, there are periods of more disease activity followed by times of remission. But with progressive MS, there is a worsening progression of the disease without clear times of remission.
Previously, MS was thought of in one of two ways: either as only having inflammation damaging the nervous system or as a disease that starts as inflammation-based and then progresses to a neurodegenerative disease. The researchers in The Lancet found that inflammation serves as a trigger as well as a driving force throughout the disease process. In addition, they posit that neurodegeneration continues even into the last stages of this disease.
The researchers suggest that the neurodegeneration of MS involves four key elements which have significant interaction with each other:
- Microglia (cells in the brain and spinal cord) activation
- Chronic free radical damage
- Accumulated damage to the mitochondrial areas of axons (nerve cells)
- Iron build-up in the brain (which tends to happen over time)
With these four areas in mind, the treatment for progressive MS in the future will likely focus on strategies to reduce inflammation, regenerate neurons, and protect neurons from damage. Yet any medication will need to be able to cross the blood-brain barrier. Another issue is that any anti-inflammatories would ideally target central nervous system inflammation. The Centre for Brain Research scientists suggest that it could be useful to minimize free radical damage or bolster antioxidant defenses in those with progressive MS. The fact that there is not a suitable animal model for progressive MS has limited the testing of these ideas.
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Mahad DH, Trapp BD, Lassmann H. Pathological mechanisms in progressive multiple sclerosis. The Lancet 2015;14(2):183-93.