As well as the cholesterol/oxysterol and PE/PC pathways defined here, accumulating evidence identifies disturbances in sphingolipid (in particular glycosphingolipid) metabolism in a growing number of neurological diseases including HSP/MND (e.g. FA2H, B4GALNT1) (Harlalka et al., 2013) and GBA2 (Sultana et al., 2015), which may potentially involve disruption of myelin integrity. This evidence concerns the gene GBA2 and hereditary spastic paraplegia.