Inhibition of alpha(4)beta(1) integrin blocks immune cell influx into the CNS providing benefit to patients with multiple sclerosis and in animal model systems. We have used this mechanism to examine whether the presence of inflammatory cells suppresses spontaneous myelin repair in experimental autoimmune encephalomyelitis. We observed (1) 87% of plaques showed remyelination after 40 days of treatment; (2) myelin repair occurred in half of the total lesion area; (3) half of the animals regained motor function. There was no significant repair or gain of motor function in vehicle-treated animals. Therefore, prolonged inhibition of CNS inflammation, in the absence of targeted myelin repair, facilitates mechanisms of spontaneous remyelination
You keep telling TeamG to get off its bum and start reporting on repair strategies. However this study suggests that one of the most important strategies to promote repair is to stop further damage occurring and then let the natural repair mechanisms kick in.
This was shown using tysabri is EAE. The big question is does this happen in MS?
The answer should be to hands. Some pathologists could have the answer, but have they looked?
Tysabri can be very effective at stopping MRI lesions and relapses,which should allow repair to occur if this is the case.
Unfortunately Tysabri also kills some MSers because of PML. Therefore how many demyelinated MS lesions are there compared to how many lesions that are remyelinated. This can determine if effective tysabri allows remyelination, or is demyelination persistent?
There clearly are some demyelinated lesions in PMLers based on one study but have pathologists really looked for remyelination.
This is an experiment that needs doing urgently!
Labels: PML, remyelination