Here is an article written by the doctor that treated Ann Romney (Howard Weiner from Harvard):http://www.ncbi.nlm.nih.gov/pubmed/19334069
The challenge of multiple sclerosis: how do we cure a chronic heterogeneous disease?
SourcePartners Multiple Sclerosis Center, Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. email@example.com
Multiple sclerosis is (MS) a T-cell autoimmune disease characterized by a relapsing-remitting followed by a progressive phase. Relapses are driven by the adaptive immune system and involve waves of T helper cell 1 (Th1), Th17, and CD8 cells that infiltrate the nervous system and provoke a attack. These cells are modulated by regulatory T and B cells.
Infiltration of T cells into the nervous system initiates a complex immunological cascade consisting of epitope spreading, which triggers new attacks, and activation of the innate immune system (microglia, dendritic cells, astrocytes, B cells), which leads to chronic inflammation. The secondary progressive phase is due to neurodegeneration triggered by inflammation and is driven by the innate immune system. Why a shift to the progressive stage occurs and how to prevent it is a central question in MS. Effective treatment of MS must affect multiple disease pathways: suppression of proinflammatory T cells, induction of regulatory T cells, altering traffic of cells into the nervous system, protecting axons and myelin, and controlling innate immune responses. Without biomarkers, the clinical and pathological heterogeneity of MS makes treatment difficult. Treatment is further hampered by untoward adverse effects caused by immune suppression. Nonetheless, major progress has been made in the understanding and treatment of MS. There are three definitions of cure as it applies to MS: (1) halt progression of disease, (2) reverse neurological deficits, and (3) prevent MS. Although the pathways to each of these cures are linked, each requires a unique strategy.
Curing Multiple Sclerosis
Immunotherapy to Halt Disease Activity and Progression
One could argue that a cure is a treatment that eradicates MS. This may be true for an infection or tumor but not for MS in which there is an inherent defect of
the immune system and chronic inflammation of the brain. If, however, one treated MS at the clinical onset and prevented disease progression for the remainder of
the patient’s life, it would be considered a cure. There may be patients who are being “cured” with current therapy, though they may have less severe forms of the
disease. Interferons and glatiramer acetate are only partially effective in MS, with stronger effects observed with natalizumab and alemtuzumab.This raises a
central question: Will aggressive and early immunotherapy prevent the secondary progressive form of the disease? With the strong antiinflammatory effects of a
drug such as alemtuzumab, this question could be addressed in the future, though widespread testing may be prohibited by adverse effects. Other approaches of
aggressive immunotherapy at disease onset to test this hypothesis include bone marrow transplantation, nonablative chemotherapy utilizing cyclophosphamide, or
induction with a drug such as cyclophosphamide or mitoxantrone followed by maintenance immune modulation. We found that a short course of cyclophosphamide
was very effective in shutting down disease activity in early aggressive MS, but less effective in older patients who had entered the later progressivestages. This
phenomenon was also observed in trials of beta interferon in progressive MS and with other anti-inflammatory drugs such as alemtuzumab and rituximab.
Patients most likely to respond to drugs with anti-inflammatory actions are those with active disease progression and adaptive immune activity as evidence
by continued relapse activity.
So, you can see many researchers within the mainstream medical community working on MS believe that the immune system is at fault and that it is neccessary to stop the inflamitory process before neurodegeneration occurs, such as using chemotherapy or HSCT protocols. These essentially re-set the immune system because of defects that have been acquired due to genetics and environment.
But one thing that is becomming clear, the immune system is faulty. In particular the Regulatory T-cell (or Treg) whose job is it to monitor the immune system and shut-down autoimmunity when it happens. Every persons immune system will attack its own tissue, but a person with healthy regulatory T-cells will stop this process when this occurs.
This is not only the case with MS, but is also true for other autoimmune diseases. For those interested in regulatory T-cells, their history and how they are trying to be manipulated in diabetes, here is an excellent video that explains this by Dr. Jeffery Blustone of the University of California:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565852/
And here is a company that is also using regulatory T-cells to develop therapies for Diabetes as well as MS:http://www.txcell.com/index.php?option=com_content&task=view&id=60&Itemid=115
So, this is where I believe science is going with MS.