IFNG and Alzheimer disease: Both the observed decline in bulk sphingolipids, as well as the shift from VLC-FA species towards sphingolipids bearing shorter-chain fatty acids parallels reported IFNγ-induced cutaneous abnormalities, previously proposed to account for the permeability barrier abnormality in AD [85], also accounting for the emergence of ultrastructural features that mimic AD (Additional file 1: Fig. S3).