Well, they don’t know for sure what our current DMD’s are doing for us, BUT they have proven scientifically that they have the potential to reduce inflammation for some people. What else they might be doing, and/or why, no one really knows.

However, in spite of their effect on a reduction to relapses and/or inflammation, the DMD’s don’t influence ‘disability progression’ to the same degree. For many, they continue to progress with disability at exactly the same pace, even though they appear to be more stable (i.e. less relapses and visible lesions).

So, there is clearly something else to the disease process that the DMD’s aren’t necessarily influencing. The current theory is neurodegeneration, and this is what this Pubmed article is referring to, particularly in the last sentence . . .

"A number of recent magnetic resonance imaging studies have challenged the classical view of multiple sclerosis (MS) as a "two-stage" disease where an early inflammatory demyelinating phase with focal macroscopic lesions formed in the white matter (WM) of the central nervous system is followed by a late neurodegenerative phase, which is believed to be a mere consequence of repeated inflammatory insults and irreversible demyelination. These studies have consistently shown the presence of diffuse normal-appearing WM damage, marked gray matter involvement and significant cortical functional reorganization, as well as the occurrence of the neurodegenerative component of MS from the earliest clinical stages of the disease with only a partial relation to MRI markers of inflammatory demyelination. The present review argues that MS can no longer be viewed as a "two-stage" disease, which suggests that the two pathological components are dissociated in time, but rather as a "simultaneous two-component" disease, where the relative contributions of the various pathological processes of the disease to the development of "fixed" disability, their relationship and their evolution over time need to be clarified. This new view of MS should inform the development of future research protocols to define its actual physiopathology and prompt the institution of early treatment which should ideally target not only inflammatory demyelination, but also the neurodegenerative aspects of the disease, as well as promote neuroprotection and enhance reparative mechanisms and adaptive functional reorganization of the cortex."

Cherie