Glial progenitor-based repair of demyelinating neurological diseases

Abstract

Demyelinating diseases of the brain and spinal cord affect more than one-quarter million of Americans, with numbers reaching more than two million across the world. These patients experience not only the vascular, traumatic, and inflammatory demyelinations of adulthood but the congenital and childhood dysmyelinating syndromes of the pediatric leukodystrophies. Several disease-modifying strategies have been developed that slow disease progression, especially in the inflammatory demyelinations and in multiple sclerosis in particular. Yet, currently available disease modifiers typically influence the immune system and are neither intended to nor competent to reverse the structural neurologic damage attending acquired demyelination. Fortunately, however, the disorders of myelin lend themselves well to attempts at structural repair, because central oligodendrocytes are the primary, and often sole, victims of the underlying disease process. Given the relative availability and homogeneity of human oligodendrocyte progenitor cells, the disorders of myelin formation and maintenance may be especially compelling targets for cell-based neurologic therapy.