While limited by the small number of patients in subgroups and aggregation of patients based on traditional clinical phenotyping, the results suggest diverging degrees and temporal patterns of myelination in PMD subtypes, namely [1] very little myelin and early loss of myelin signal in severely affected connatal and classic patients [3], more, though still severely deficient myelin in classic PMD [4], ongoing myelination in classic and intermediate PMD during childhood [5], potential early loss in PLP0 and later loss in female and SPG2 patients. Here, PLP1 is linked to Pelizeaus-Merzbacher spectrum disorder.