Nervous/immune systems: Demyelinating disease

Multiple sclerosis (MS) is an autoimmune condition that leads to selective demyelination of the central nervous system. In patients with MS, multifocal plaques, or zones of demyelination, can be seen throughout the white matter of the brain and spinal cord.

The pathogenesis of the disease involves an immune attack against CNS antigens mediated through activated CD4+ myelin-reactive T cells. Our understanding of the immunopathogenesis of MS has been informed by experimental autoimmune encephalomyelitis (EAE), an animal model of CNS inflammatory demyelination that can be induced by peripheral immunization with myelin protein components. EAE shares many of the histologic features of MS, including active demyelination and axonal loss, all of which are presumably mediated by myelin-specific T cells.

Researchers are examining the effects of demyelination in EAE prior to neuronal injury or loss. To do this, they compare in vitro conduction velocities of four groups of nerve samples: spinal cord samples isolated from a group of normal, healthy rats, spinal cord samples isolated from a group of rats with EAE, and two control groups derived from lab-prepared materials that serve positive and negative controls. One of these controls accurately mimics a highly myelinated nerve; the other, a completely demyelinated nerve. The samples are suspended between two electrodes in solution. A small current is applied to one electrode and the voltage is measured as a function of time at the other electrode; from this measurement, the conduction velocity of each nerve sample can be determined. Figure 1 shows mean conduction velocities versus nerve diameter for each test group.

Figure 1 Mean conduction velocities with respect to axon diameter for test groups A–D