Remyelination in Multiple Sclerosis is halted because the immune system attacks myelin. This remyelination in MS stops working as the body produces a type of an inflammatory response that ultimately causes demyelination. However, research done by Dr. Rodriguez and his team using experiments done on laboratory mice, this inflammation that demyelinates axons can also induce a process of repair called remyelination. This is what explains an apparent paradox of the laboratory mice improving in health when this inflammation was induced. Remyelination was fairly limited and patchy in the mice that were tested, but it did actually occur. The question that needed to be answered was if this process also occurs in humans, and if it does, could that process be harnessed for treatment of MS?

It is due to these findings that Dr. Lucchinetti, along with an international group of collaborating scientists in the MS Lesion Project, studied over 700 people worldwide with MS who had undergone brain biopsies. Using these tissue samples, the scientists discovered actual evidence of remyelination in humans. They also discovered four unique patterns of tissue destruction in MS. These four subtypes can explain the variability of symptoms between different patients. Two of these MS patterns did show evidence of strong natural remyelination. However, other two did not. The scientists also found that strong remyelination that occurred in the early-stage MS did not always mean good remyelination would occur later on.


Antibody Number 22


Remyelination helps to keep axons alive and this may protect against the irreversible progression of this disease. The earliest thinking about the therapeutic uses of remyelination focused on cell transplantation and growth factor strategies. However, both of these methods tested proved disappointing. Research by Dr. Rodriguez focused on search for a natural human autoantibody, or immune-based protein that can promote the natural repair they discovered.

A breakthrough occurred in 2001 when Dr. Rodriguez and his colleagues uncovered what is known as Antibody Number 22.  Key features of 22 are that it is larger and different in shape from other antibodies. Most importantly, this antibody belongs to the body, is found in many different species, and is actually thought to be very old and primitive in terms of evolution. This particular autoantibody is the initial defense the body sends out against viruses. Another key factor is that it carries few if any side effects, unlike industry-synthesized antibodies. Researchers identified this autoantibody in a patient and set about the task to sequence, reproduce, and test it.

They found that this promoted remyelination in Multiple Sclerosis in approximately 50% of lesions in laboratory mice that were infected with a virus that mimics MS. Along with this, the remyelination in MS was effectively caused in greater than 85% of animals tested, which sparked interest in scientists to hope for human trials relatively soon.