Duplication boundaries have now been mapped in a large collection of ADLD families, confirming that the minimal duplicated regions necessary for the disease includes the whole of the LMNB1 gene, which can be inverted, and that probably arose through non-homologous end joining or replication-based defects [65]. Here, LMNB1 is linked to adult-onset autosomal dominant demyelinating leukodystrophy.