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BookmarkScienceDaily (Dec. 22, 2008) — Multiple sclerosis (MS) is an inflammatory disease of the brain and spinal cord that progresses overtime, with increasing disability. It occurs when the immune system inappropriately attacks both the sheath that insulates and protects the nerve cells and the cells that make this sheath, oligodendrocytes.
One question regarding the disease is why precursors of oligodendrocytes are still present in diseased areas of the brain of individuals with MS but do not develop into oligodendrocytes and produce the nerve cell sheath. However, Jin Nakahara and colleagues, at Keio University School of Medicine, Japan, have now provided insight into this issue through analysis of brain tissue from MS patients and rodent cell lines in vitro.
In the study, damaged nerve cells in diseased areas of the brain of individuals with MS were found to express high levels of the protein Contactin, which interacted with the protein Notch1 on precursors of oligodendrocytes. In normal tissues, this triggers a signaling pathway that induces the precursors to develop into oligodendrocytes. However, in the diseased areas of the brain of individuals with MS these signaling events did not occur normally. Specifically, a protein known as TIP30 was abnormally overexpressed, preventing a key signaling component (the Notch1 intracellular domain) from performing its function. The authors therefore conclude that this signaling defect contributes to the development of MS.
In an accompanying commentary, Celia Brosnan and Gareth R. John highlight the key aspects of the study and discuss the implications for our understanding of MS.
Story Source:
Adapted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Journal Reference:
- Nakahara et al. Abnormal expression of TIP30 and arrested nucleocytoplasmic transport within oligodendrocyte precursor cells in multiple sclerosis. Journal of Clinical Investigation, Dec 22, 2008; DOI: 10.1172/JCI35440
Note: If no author is given, the source is cited instead.
