More MS news articles for Oct 2001

TNF-Alpha May Have Dual Role in Demyelinating Diseases

WESTPORT, CT (Reuters Health) Oct 15 - Tumor necrosis factor-alpha (TNF-alpha) exacerbated acute demyelination in a mouse model of multiple sclerosis, according to a report in the November issue of Nature Neuroscience. During the recovery process, however, TNF-alpha accelerated the production of oligodendrocyte precursors and mature oligodendrocytes in wild-type mice.

"Our study...may help explain the seemingly conflicting roles of TNF-alpha in demyelinating diseases," Dr. Jenny P.-Y. Ting, of the University of North Carolina at Chapel Hill, and colleagues propose.

The researchers induced demyelination using cuprizone, a neurotoxin, in wild-type mice and in mice lacking the TNF-alpha gene. In the TNF-alpha knockout mice, demyelination and oligodendrocyte apoptosis were delayed by a "modest but statistically significant" amount compared with wild-type mice.

After removal of cuprizone from their diets, the wild-type mice exhibited rapid remyelination. "After 2 weeks of recovery, only 11.0% of axons in the wild-type mice remained demyelinated compared with 78.4% of axons in mice lacking TNF-alpha," the investigators report.

Examination of B cells showed that the remyelination due to TNF-alpha was not due to B-lymphocyte-mediated processes. The fact that the knockout mice were slower to repair the damage suggests that proliferation of oligodendrocytes requires TNF-alpha signals, the researchers suggest in a statement released Monday.

Therefore, Dr. Ting's group proposes, the timing of treatment with TNF-alpha may affect the efficacy of the treatment.

Nat Neurosci 2001;4:1116-1122.

Copyright © 2001 Reuters Ltd