What is it about?
Multiple sclerosis (MS) is an immune disease that damages myelin, the protective insulation around nerve fibers in the brain and spinal cord. Although the body has a natural mechanism for repairing this damage, it often fails over time, leading to permanent nerve damage and disability. This study found that blood vessel cells control repair via a protein called TNFR2; without it, vessels overproduce another protein called fibronectin, trapping repair cells and blocking myelin rebuilding. Blocking fibronectin restored repair and improved symptoms revealing blood vessels as a new therapeutic target for MS.
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Photo by Markus Kammermann on Unsplash
Why is it important?
Our findings show that targeting blood vessels can reshape the environment inside the brain and spinal cord to allow nerve repair. This is particularly significant because delivering therapies across the blood–brain barrier remains one of the major challenges in treating neurological disorders. By targeting blood vessel cells, which are directly accessible from the bloodstream, we may be able to overcome this obstacle. Additionally, while current MS treatments focus on controlling inflammation, our approach directly promotes remyelination, a repair-based strategy that could be used alongside existing therapies.
Perspectives
Our mouse model findings suggest that targeting blood vessels with fibronectin inhibitors could offer genuine therapeutic value. I'm particularly focused on identifying mechanisms with real translational potential, and I believe vascular-targeted therapy could open exciting new avenues of research and be a game changer for MS treatment.
George Kollias
Biomedical Sciences Research Center Alexander Fleming
What is particularly fascinating is that blood vessels do more than deliver oxygen, nutrients and immune cells to the central nervous system. They actively regulate the surrounding neural tissue shaping its cellular landscape. By influencing neighboring cells and repair signals, blood vessels can create a repair-permissive environment that promotes myelin regeneration highlighting their potential as therapeutic targets for a range of neurological diseases.
Aikaterini Nanou
Biomedical Sciences Research Center Alexander Fleming
Read the Original
This page is a summary of: Fibronectin inhibition restores myelination in endothelial TNFR2–dependent nonremitting experimental autoimmune encephalomyelitis, Proceedings of the National Academy of Sciences, September 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2616799123.
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