Studies in both humans and experimental animals have demonstrated that myelin repair in the CNS is a normal physiological response to myelin damage, similar to tissue injury elsewhere in the body. The unanswered question is why myelin repair is incomplete in multiple sclerosis patients. In this paper we review the morphological characteristics of remyelination, discuss the available animal models of CNS demyelination and their usefulness to identify the molecular, cellular, and morphological events involved in CNS myelin repair, examine the use of immunosuppression, immunoglobulins, protein growth factors, and glial cell transplantation as the primary experimental therapies designed to promote CNS remyelination, and address the potential electrophysiological and clinical benefits of myelin repair in the CNS.
|Original language||English (US)|
|Number of pages||14|
|State||Published - Jul 1996|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Clinical Neurology