Journal
JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 265, Issue 1-2, Pages 5-11Publisher
ELSEVIER
DOI: 10.1016/j.jns.2007.09.007
Keywords
multiple sclerosis; inflammation; demyelination; myelin; EAE
Categories
Funding
- NINDS NIH HHS [NS08952, NS 11920] Funding Source: Medline
- CSR NIH HHS [RG 1001-J-10] Funding Source: Medline
Ask authors/readers for more resources
In multiple sclerosis (MS), myelin destroyed by the immune attack is not effectively repaired by oligodendrocytes (OLs) and MS foci eventually undergo glial scarring. Although oligodendrocyte precursor cells (OPCs) are normally recruited to the lesion areas, they fail to mature and remyelinate the damaged fibers. Activation of the Notch pathway has been shown to inhibit OPC differentiation and to hamper their ability to produce myelin during CNS development. We have recently shown that inhibition of gamma-secretase within the CNS of SJL/J mice with experimental autoimmune encephalomyelitis (EAE) blocks Notch pathway activation in OLs, promotes remyelination, reduces axonal damage and significantly enhances clinical recovery from the disease. Our results suggest that inhibiting the non-myelin permissive environment maintained by Notch pathways within the mature CNS offers a new strategy for treating autoimmune demyelination, including MS. (C) 2007 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available