Starting with transplants of human oligodendrocytes in the late 1980s [40], and more recently with populations of human oligodendrocyte progenitor cells isolated from the developing or adult CNS, or from human embryonic stem cells, it has been possible to generate extensive myelination upon transplantation into spinal cord injury or into congenital mouse models of hypomyelination [41]--[48]. (journals.plos.org)
Although genetic deletion of BACE1 results in abolished amyloid pathology in AD model mice, it also results in neurodevelopmental phenotypes such as hypomyelination and synaptic loss, observed in schizophrenia and autism - like phenotype. (content.iospress.com)