In the central nervous system (CNS), oligodendrocytes (OL) support neuronal health and function by extending myelinating processes and providing trophic and metabolic support to the underlying axon1,2. OLs are derived from the differentiation of oligodendrocyte progenitor cells (OPCs) throughout the lifespan3–7. However, most are generated in early development, within the first decade in humans and before 2 months of age in mice. Tracking of OL dynamics under homeostasis has indicated 100-fold more annual OL turnover in mice (>36%) vs humans (0.3%)7. What is consistent between species, however, is the highly dynamic turnover of myelin4,5,7. Injury to, and loss of, mature OLs and their processes are a prominent feature of myelin damage (demyelination) underpinning an array of clinical disorders across the lifespan.
