The team led by Kerschensteiner and Misgeld set out to define
precisely how the damage to the nerve axons occurs. As Misgeld explains,
"We used an animal model in which a subset of axons is genetically
marked with a fluorescent protein, allowing us to observe them directly
by fluorescence microscopy." After inoculation with myelin, these mice
begin to show MS-like symptoms. But the researchers found that many
axons showing early signs of damage were still surrounded by an intact
myelin sheath, suggesting that loss of myelin is not a prerequisite for
axonal damage.

Instead a previously unrecognized mechanism, termed focal axonal
degeneration (FAD), is responsible for the primary damage. FAD can
damage axons that are still wrapped in their protective myelin sheath.
This process could also help explain some of the spontaneous remissions
of symptoms that are characteristic of MS. "In its early stages, axonal
damage is spontaneously reversible," says Kerschensteiner. "This finding
gives us a better understanding of the disease, but it may also point
to a new route to therapy, as processes that are in principle reversible
should be more susceptible to treatment."

However, one must remember that it takes years to transform novel
findings in basic research into effective therapies. First the process
that leads to disease symptoms must be elucidated in molecular detail.
In the case of MS it has already been suggested that reactive oxygen and
nitrogen radicals play a significant role in facilitating the
destruction of axons. These aggressive chemicals are produced by immune
cells, and they disrupt and may ultimately destroy the mitochondria.
Mitochondria are the cell's powerhouses, because they synthesize ATP,
the universal energy source needed for the build-up and maintenance of
cell structure and function.

摘錄自http://www.sciencecodex.com/a_possible_new_target_for_treatment_of_multiple_sclerosis