The use of cultured autologous Schwann cells to remyelinate areas of persistent demyelination in the central nervous system.
Areas of persistent demyelination were created in the dorsal columns of the cat spinal cord by injecting ethidium bromide into white matter which had previously been exposed to 40 Grays of X-irradiation. In the centre of such lesions demyelinated axons occurred in a glial-free area while axons next to normal tissue were separated by astrocyte processes. No remyelination occurs in such lesions (Blakemore 1984). Autologous Schwann cells and fibroblasts cultured from a peripheral nerve biopsy were injected into such lesions and the extent of Schwann cell remyelination examined. Only lesions injected with viable cells showed remyelination by Schwann cells; in no lesion were all the demyelinated axons remyelinated. Three forms of association of Schwann cell with axons were detected. In the centre of the lesions Schwann cells either remyelinated axons around or near to blood vessels, or lay next to demyelinated axons and did not form myelin. Schwann cell remyelination was also detected in the astrocyte-containing areas around the edges of some lesions. It was concluded that the extent of Schwann cell remyelination was influenced by the mode of entry of the cells into the lesion and by the architecture of the lesion. The presence or absence of stable extracellular matrix is believed to be the prime factor which influenced Schwann cell remyelination. The relevance of these observations to artificial repair of the lesions of multiple sclerosis is discussed.