Key result
Manipulation of the immune response in experimental models indicates potential to promote endogenous CNS remyelination and functional recovery in Multiple Sclerosis.
Why the study?
Does manipulation of the immune response promote endogenous CNS remyelination and functional recovery in Multiple Sclerosis?
Does manipulation of the immune response promote endogenous CNS remyelination and functional recovery in Multiple Sclerosis?
Manipulation of the immune response in experimental models suggests potential for promoting endogenous CNS remyelination and functional recovery in Multiple Sclerosis.
Answers are grounded in this paper and cite their sources.
Remyelination remains incomplete in MS; leaves open whether targeting repair factors improves outcomes.
Studies in both human and experimental models demonstrate that myelin repair occurs in the central nervous system and is a normal physiologic response to myelin injury. However, remyelination in MS is often incomplete and limited. The outcome of an actively demyelinating lesion depends on the balance between factors promoting myelin destruction and myelin repair. Experimental models of CNS demyelination provide an opportunity to investigate the morphologic, cellular and molecular mechanisms involved in remyelination. This review focuses on experiments using the Theiler's virus model of demylination which indicate that manipulation of the immune response has the potential to promote endogenous CNS remyelination and functional recovery in MS.
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Lucchinetti et al. (1997) conducted a review in Multiple Sclerosis. Manipulation of the immune response was evaluated on Endogenous CNS remyelination and functional recovery. Manipulation of the immune response in experimental models indicates potential to promote endogenous CNS remyelination and functional recovery in Multiple Sclerosis.
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