However, a major challenge in this study was that although lipid classes and their proportions were similar between species (mice and human), the pathological causes of the diseases were totally different, i.e., mutated APP/PS1 genes in mice and non-genetic multifaceted in sporadic human AD, both conveyed in the development of amyloid histopathology [35,36,37]. This evidence concerns the gene PSEN1 and amyloidosis.