We study a specialized glial cell, the oligodendrocyte, which myelinates axons in the brain and spinal cord. The laminin family of adhesion proteins are good candidates to regulate oligodendrocytes and the process of myelination: brain defects, including abnormal myelination, occur in the absence of normal laminin signaling. Our work has demonstrated that adhesive interactions with laminins can stimulate oligodendrocytes to survive and differentiate, at least in part by altering interactions with growth factors and downstream signal transduction mechanisms. We are now learning how laminins and laminin-regulated signaling molecules operate during normal brain development and function, as well as during diseases where myelination is dysregulated. An understanding of the mechanisms that control myelination will be important for two areas of human health: (1) during development, where normal myelination is crucial, and (2), during brain and spinal cord repair, which is hampered by the inability of the central nervous system (CNS) to regenerate. Remyelination failure leads to the neurodegeneration in demyelinating diseases such as Multiple Sclerosis, and is predicted to play a role in the neurodegeneration process in diseases such as Alzheimer’s, and, following CNS injury in which new neuronal connections need to be myelinated to achieve functional recovery. One of our long-term objectives is to design pharmacological strategies to enhance myelination and myelin repair in the damaged nervous system.