PLXNB3 and Alzheimer disease: We hypothesize that such mechanisms may be largely disrupted in AD (Supplementary Fig. 14); nevertheless, further studies are clearly needed to understand the fundamental mechanisms of adult cortical myelination, the roles of plexin-B3+ aOPCs in health and disease, the pathophysiology of AD-type de- or dysmyelination, and the possible corresponding therapeutic interventions.