Steinman L, Zamvil SS. Beginning of the end of two-stage theory purporting that inflammation then degeneration explains pathogenesis of progressive multiple sclerosis. Curr Opin Neurol. 2016. [Epub ahead of print]
PURPOSE OF REVIEW:The review discusses future directions in research on multiple sclerosis and neuromyelitis optica, as long-held beliefs about these diseases are undermined with data from recent clinical trials.
RECENT FINDINGS: Results of clinical trials for registration (phase 3) were reported in the last year. Anti-inflammatory approaches, such as daclizumab high-yield process targeting IL-2 receptor, and ocrelizumab targeting CD20 B cells, confirmed a beneficial role of immune suppression in relapsing-remitting disease. And now for the first time achieving the primary end point in primary progressive multiple sclerosis was attained with ocrelizumab.
SUMMARY: The results in the past year challenge the long-held belief that relapsing-remitting disease is inflammatory, whereas progressive forms of the disease are 'less inflammatory' and more 'degenerative.'
Well the tide is changing, some people have believed that all aspects of MS are a problem of autoimmunity...largely T cell autoimmunity. Then came along rituximab and ocrelizumab and MS, and slowly EAE becomes a B cell disease. If this is true surely the end of progressive MS is nigh.
The hint of efficacy of ocrelizumab in PPMS now means that the idea that progressive MS harbours a neurodegenerative process is going to be dismissed according to this new view.
Is this going to be the new world view.
Personally I would not be too hasty to do this as all you have to do is actually look in progressive MS and you can see that it indeed progressive MS is less inflammatory and there is nerve loss.
The trial with ocreluzimab was loaded with potential responders but it did not halt progresive MS so in my opinion not yet time to relax, we need to do better.
So one swallow does not a summer make unless you live in California I guess :-)
Labels: progressive MS