APP and Alzheimer disease: In a lipidomic analysis where human late-onset AD brain tissue was compared to transgenic familial-AD (FAD) mouse-models with mutations in presenilin 1 (PS1) and APP genes, the authors show that, although many lipid alterations were different between the two models, ganglioside (GM3) and cholesterol esters (CE; components of circulating lipoproteins), in particular, showed that disease-related alterations in brain concentration were comparable between the human and animal model [93].