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Sunday, September 17, 2017 6:45 PM | CCSVI in Multiple Sclerosis Volg link
David Hubbard
September 16, 2017
Alliant International University

A new model of MS pathogenesis is reviewed in which the primary mechanism is not immunopathology but instead blood-brain barrier disruption and hypoperfusion: “The focus on the peripheral immune system alone may be limiting our understanding of the disease and the success of developing therapies.” The authors note that all current immunomodulatory therapies act on downstream immune-mediated pathology and provide no treatment for progressive disease or cure. A review of research demonstrates that BBB disruption is present at the earliest stages of disease, preceding symptoms, enhancing lesions, or other MRI changes. Global hypoperfusion is present before any grey matter volume loss and is out of proportion to reduced metabolic demand associated with axonal loss. They propose that oxidative stress secondary to chronic hypoxia causes oligodendrocyte degeneration and selective myelin loss which then leads to immune cell infiltration secondarily.

Finally, the diagnosis and treatment of MS shifts from suppressing T-cells and to perfusing oligodendrocytes.

https://www.researchgate.net/publication/319422370_Vascular_pathology_in_multiple_sclerosis_reframing_pathogenesis_around_the_blood-brain_barrier
Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier
On Aug 31, 2017 Jonathan I Spencer (and others) published: Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier