Demyelinating disorders, or leukodystrophies, cause nervous system deficits owing to breakdown of the myelin sheath, which is essential for rapid and efficient neuronal communication. Prior studies of adult-onset autosomal dominant leukodystrophy (ADLD) have identified that the structural protein lamin B1 plays a role in maintaining myelin. Here, Shu-Ting Lin and Ying-Hui Fu further investigate the mechanisms by which expression of the lamin B1 gene, LMNB1, influences myelin integrity. They found that overexpressed lamin B1 halts the development of oligodendrocytes which form and maintain myelin in the central nervous system. They also identified a microRNA miR-23, which tightly regulates lamin B1 protein levels, as a potential therapeutic target in combating demyelinating disease.
