Some of the nontumor problems of NF1 patients, such as learning disabilities, hydrocephaly and UBOs (unidentified bright objects identified by MRIs thought to represent areas of hyper-myelination), have led us, in collaboration with Tilat Rizvi, PhD, to discover the abnormalities of oligodendrocyte development in the NF1 mouse models. Oligodendrocytes myelinate the axons in the CNS, providing an increased conductivity for the electrical nerve impulses traveling through the axons. Examining how oligodendrocytes develop may provide potential therapies not only for NF1 patients, but also for patients with multiple sclerosis (a disease in which axons become demyelinated).