Lipidomics analyses of the frontal cortex of frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) patients had shown a marked disruption of lipid homeostasis, in particular a reduction in key lipid species such as ether lipids and acylcarnitines, which are essential for maintaining myelin integrity and neuronal function [2, 13]. This evidence concerns the gene TARDBP and frontotemporal dementia.