Research from Dr. Ian Duncan, University of Wisconsin

Dr. Ian Duncan’s group from the University of Wisconsin summarized three new (and as yet unpublished) projects. Two of them involved research on a mutant mouse (op) that is not able to develop certain cell types that are important in bone remodeling and in the immune system.

The first project studied the numbers of microglial cells, which are part of the immune system in the central nervous system. The microglia are important in diseases of brain inflammation, such as multiple sclerosis. Dr. Duncan’s lab found that there are fewer microglial cells in the white matter of op mice as compared to control mice. However, the numbers of microglia in the grey matter were not different between the two groups. While microglia in both mutant and control mice responded to a wound in the cerebral cortex (part of the brain grey matter), the change in the op mice was less than the control. These findings make the op mouse a useful model in which to explore the role of microglia in inflammatory diseases.

The second project on the op mouse studied the optic nerve. Because op mice have abnormal bone remodeling, the surrounding bone compresses their optic nerve. At the compression site, there are few oligodendrocytes, the cells that make brain myelin. So, there is little or no myelination at this site. Nerve conduction through the area of non-myelination is severely affected. The group plans to study whether the oligodendrocytes die because compression reduces their blood supply.

Finally, Dr. Duncan reported on a new model of chronic demyelination and remyelination in the cat, induced by feeding the animals an experimental diet. Only the myelin sheath appears to be affected, with axons remaining intact. When the cats are returned to a normal diet, they recover neurologically with evidence of remyelination throughout the entire CNS. This model proves unequivocally, and for the first time, that remyelination restores function in a large animal model and confirms that remyelination is a major therapeutic target in demyelinating disease.